Since the causative agent, SARS-CoV-2, is a recently discovered species, there is no specific medicine for downright treatment of the infection. This has led to an unprecedented societal fear of the newly born disease, adding a psychological aspect to the physical manifestation of the virus. Herein, the COVID-19 structure, epidemiology, pathogenesis, etiology, diagnosis, and therapy have been reviewed.

Probiotics have shown promising results for curing skin-influencing inflammatory disorders through modulating the immune response by manipulating the gut microbiome.

GPR81 (also named as HCA1) is a member of a subfamily of orphan G-protein coupled receptors (GPCRs), coupled to G_i-type G proteins. GPR81 was discovered in 2001 and identified as the only known endogenous receptor of lactate under physiological conditions in 2008, which opened a new field of research on how lactate may act as a signal molecule along with the GPR81 expression in roles of metabolic process and inflammatory response. Recent studies showed that the physiological functions of GPR81 include lipid metabolism in adipose tissue, metabolic excitability in the brain, cellular development, and inflammatory response modulation. These findings may reveal a novel therapeutic strategy to treat clinical, metabolic, and inflammatory diseases. This article summarizes past research on GPR81, including its characteristics of distribution and expression, functional residues, pharmacological, and physiological agonists, involvement in signal transduction, and pharmacological applications.

Recent studies have reported the anticancer activity of biosynthesized gold nanoparticles (Au-NPs), especially in lung cancer. This review focused on the advances in the antilung cancer activity of biosynthesized Au-NPs and its potential mechanisms.

This review summarizes and analyzes the updated information on the regulation of sortilin expression and its trafficking function. Recent advances in the regulation of sortilin expression and function, and its related mechanisms will help the ongoing research related to sortilin and promote future clinical application via sortilin intervention.

In this study, we assess the biochemical pathways of melanin synthesis, and the role of each gene in this pathway also has been examined in the signaling pathway that stimulates melanin synthesis.

To become leader cells, cancer cells need intrinsic properties to confer them with the potential to acquire leader cell phenotype and the support from the neighboring cells can convert the potential into specific leader cell behavior. Intrinsic properties include the distinct genetic expression, protein synthesis, and signaling cascades to promote cytoskeletal rearrangements, structural reorganization, and morphological polarization. Meanwhile, follower and stromal cells in the microenvironment can steer the potential leader cells to initiate appropriate polarization, exert leader cell behavior, and consolidate leadership by cell–cell junctions, the stimulation of multiple chemokines, and growth factors and modification of the microenvironment.

• 1.

  Inflammatory effectors and mediators can exert protective or detrimental role post-cardiac infarction.

• 2.

  Inflammatory response facilitated cardiac repair, but excessive inflammation lead to adverse left ventricular remodeling.

• 3.

  Broad-spectrum anti-inflammatory agents, may produce a short-term effect on inflammatory response, but it would cause catastrophic consequence for myocardial repair.

Cellular interactions with structurally altered ECM components may serve as cryptic signaling hubs that help control cell behavior. Selective targeting of these cryptic signaling hubs may provide novel strategies to control malignant tumor growth and metastasis.

This review summarizes the cellular and clinical implications of deletion and duplication variants of the SLC2A3 gene which encodes the glucose transporter 3. Disease associations of these copy number variants with neurodevelopmental and neurodegenerative disorders, congenital heart defects, and autoimmune diseases are discussed, focussing on how metabolic alterations may influence cellular development and degeneration.

• 1.

  circRNAs are capable of various biological functions including miRNA sponge, mediating alternatives, regulating genes at posttranscriptional levels, and interacting with proteins, indicating a pivotal role of circRNA in osteosarcoma initiation, progression, chemoresistance and immune response.

• 2.

  circRNAs have been thrust into the spotlight as potential biomarkers and therapeutic targets in osteosarcoma.

This review summarizes the protective mechanisms and potential therapeutic applications of H₂S in myocardial ischemia.

Summary of proposed mechanisms for participation of HULC in the pathogenesis of cancer. (a) HULC increases expression of ubiquitin-specific peptidase 22 (USP22), which reduces ubiquitin-induced degradation of COX-2 protein by eliminating the conjugated polyubiquitin chains from COX-2 and increasing stability of COX2 protein. (b) HULC interacts with EZH2 to inhibit expression of NKD2, a negative regulator of Wnt signaling. (c) HULC participates in ZEB1-induced epithelial–mesenchymal transition (EMT) by acting as competing endogenous RNA (ceRNA) to seize miR-200a-3p signaling.

Despite the beneficial roles of hematopoietic stem cell transplantation (HSCT) in hematologic malignancies, relapse is still a nettlesome challenge. Hematologic cancer cells induce exhaustion in immune cells through several mechanisms, such as inhibitory immune checkpoints, which lead to immune escape and relapses after HSCT. We reviewed the clinical roles of immune checkpoints in hematologic malignancies and post-HSCT relapses.

• Multiepitope vaccines that are designed by immunoinformatics methods are favorable for outbreaks of great proportions.

• The enhancing antibody problem appears to be a contributing factor in coronavirus disease-2019 (COVID-19) vaccine design.

• The broad global access for the pandemic COVID-19 vaccine, if available, should be ensured to avoid the potential of disease outbreak in the future.

The main focus of this study is the structural, mechanistic, and therapeutic studies that have been conducted to explain how heat shock protein 90 molecular chaperone and its inhibitors act on different processes involved in hepatocellular carcinoma development and progression.

This paper is intended to serve as a comprehensive repository of information on this topic and is expected to contribute to the design of other research projects and future efforts to develop treatment strategies for ameliorating the effects of CCR9/CCL25 in cancer.

In late December 2019 in Wuhan, China, several patients with viral pneumonia were identified as 2019 novel coronavirus (2019-nCoV). So far, there are no specific treatments for patients with coronavirus disease-19 (COVID-19), and the treatments available today are based on previous experience with similar viruses such as severe acute respiratory syndrome-related coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV), and Influenza virus. In patients with COVID-19, hydroxychloroquine decreases the inflammatory response and cytokine storm, but overdose causes toxicity and mortality. Neuraminidase inhibitors such as oseltamivir, peramivir, and zanamivir are invalid for 2019-nCoV and are not recommended for treatment but protease inhibitors such as lopinavir/ritonavir (LPV/r) inhibit the progression of MERS-CoV disease and can be useful for patients of COVID-19 and, in combination with Arbidol, has a direct antiviral effect on early replication of SARS-CoV. Favipiravir increases clinical recovery and reduces respiratory problems and has a stronger antiviral effect than LPV/r. Currently, appropriate treatment for patients with COVID-19 is an angiotensin-converting-enzyme 2 inhibitor and a clinical problem reducing agent such as favipiravir in addition to hydroxychloroquine and corticosteroids.

This review provides an overview of advances in surgical approaches, induction chemotherapy, radiotherapy, autologous stem-cell transplantation, salvage treatments, and novel therapeutic approaches in immunocompetent patients with primary central nervous system lymphoma (PCNSL) in the past 5 years. Additionally, therapeutic progress in elderly patients and in those with relapsed/refractory PCNSL is also summarized based on the outcomes of recent clinical studies.

In this review, we summarize iPSC-based disease modeling in neurodegenerative diseases including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Huntington's disease (HD). Moreover, we discuss the efficacy of cell-replacement therapies for neurodegenerative disease.

In the current review, we provide a brief overview of mesenchymal stromal cells (MSCs) sources, isolation, and expansion as well as immunomodulatory activities. More important, we try to collect and discuss recent Preclinical and clinical research and evaluate current challenges in the context of the MSC-based cell therapy for regenerative medicine.

At the end of December 2019, a novel acute respiratory syndrome Coronavirus 2 (SARS-CoV2) named COVID-19 emerged in Wuhan, China. Coronavirus becoming a critical challenge in global public health due to rapid development and extreme spread by active carriers in human-to-human transmission. Accordingly, there is a critical requirement for early diagnosis of COVID-19 infected or suspected cases for applying appropriate care and treatment. In this review, we comprehensively present the clinical and para-clinical diagnostic approaches to COVID-19 and their various applications, advantages, and disadvantages aspects, which would be useful for expanding perspectives and understanding more about diagnostic methods.

Wharton's jelly derived mesenchymal stem cells (WJ-MSCs) have rapidly advanced into clinical trials for the treatment of a wide range of disorders. Therefore, this paper summarized the current preclinical and clinical studies performed to investigate the regenerative potential of WJ-MSCs in neural, myocardial, skin, liver, kidney, cartilage, bone, muscle, and other tissue injuries.

Curcumin-loaded nanocarriers enhance the bioavailability, cellular uptake, and antitumor activity of curcumin. The aforementioned effects are comprehensively discussed in the current review to further direct studies for applying curcumin in lung cancer therapy.

The expression of HOTAIR has been increased in esophageal cancer. HOTAIR sponges miR-148a to increase the expression of Snail2. Snail2 has a prominent role in the induction of epithelial-to-mesenchymal transition (EMT). Moreover, HOTAIR enhances the trimethylation of H2K27 in the WIF-1 promoter through PRC2. WIF-1 is an inhibitor of the Wnt/β-catenin pathway. Thus, HOTAIR activates this pathway to further enhance EMT.

Cytokine-induced killer (CIK) cells featuring non-MHC-restricted tumor-killing activity have provided encouraging results in clinical studies. Here, we update the clinical data including a total of 106 trials enrolled in the international registry on CIK cells (IRCC) established in 2010. The recent multiple improvements both on antitumoral efficacy and toxicity make CIK cells an important therapeutic approach in clinical practice of cancer immunotherapy.

• (1)

  Immune-related long noncoding RNA (lncRNA) signature had an important value for disease progression and survival prediction in hepatocellular carcinoma (HCC)

• (2)

  Immune-related lncRNA signature may have the potential to measure the response to immune checkpoint blockade immunotherapy.

• (3)

  Our study showed immune-related lncRNA signature provided valuable clinical applications in antitumor immunotherapy in HCC.

We identified endocan as a microRNA-181a-5p target gene. miR-181a-5p/endocan regulates retinal angiogenesis through the extracellular signal-regulated protein kinases 1 and 2 signaling pathway and might represent an attractive therapeutic strategy for retinal neovascularization.

Ventricular Zone Expressed PH Domain Containing 1 (VEPH1) inhibits the differentiation of aortic smooth muscle cells (AoSMCs).

In this study, we explored the effect of glial cell line-derived neurotrophic factor (GDNF) on 1-methyl-4-phenylpyridinium-injured differentiated SH-SY5Y cells. The results showed considerable protein and lipid alterations in response to GDNF, especially altered levels of dopamine-β-hydroxylase, heat shock 70 kDa protein, neural cell adhesion molecule, cytoskeletal proteins, and long-chain polysaturated/unsaturated fatty acids. We hope these findings could reveal a new avenue to explore the relationships between GDNF, lipid rafts, and Parkinson's disease (PD) and support the hypothesis that GDNF may be a useful treatment for PD.

Long noncoding RNAs nuclear-enriched abundant transcript 1 (NEAT1) were greatly increased in patients with diabetic retinopathy (DR), in the retina of diabetic rats and mice, and knockdown of NEAT1 enhanced proliferation, repressed high-glucose (HG)-induced apoptosis, and reduced HG-triggered oxidative stress injury in human retinal endothelial cells. Furthermore, the silence of NEAT1 could reduce the enhanced expression of vascular endothelial growth factor (VEGF) and transforming growth factor-β1 (TGF-β1) induced by HG. Hence, NEAT1 might contribute to the development of DR through activating TGF-β1 and VEGF.

Our study demonstrated a novel role played by X-box binding protein 1 in modulating the viability of liver cancer cells via the Mst1-JNK-mitochondrial ROS pathways.

Kinesin family member 15 appears to be an oncoprotein that contributes to gastric cancer (GC) progression and is expected to help identify new biomarkers and treatment targets in GC.

p120 suppresses proliferation and stimulates differentiation of oral squamous cell carcinoma (OSCC) cells and the effect of p120 is mediated by inhibiting the nuclear PLC-γ1 signaling pathway. The findings might provide new potential therapeutic targets for OSCC.

The current research article comprehensively discusses the molecular mechanism between microRNA-29a-3p and phosphatase and tensin homolog (PTEN) in the development and progression of AAA. It can be understood that the PTEN was directly targeted by microRNA-29a-3p so as to regulate the AAA progression. PTEN was found to strengthen the proliferation effect of microRNA-29a-3p in AAA cells.

The mechanism by which interleukin-6 (IL-6) stimulates adrenal androgen overproduction is unknown. We found that the IL-6 can promote androgen secretion by regulating the expression of genes related to androgen pathways.

In arterial and pulmonary thrombosis mouse model, maslinic acid showed prominent anticoagulant and antithrombotic effects. Our data suggest maslinic acid as a candidate molecule for a new class of drugs targeting anti-FXa and antiplatelet.

Signal transducer and activator of transcription 3 (STAT3) has a pivotal role in cancer microenvironment. In this study, we investigate the relationships between STAT3 and programmed death-ligand 1 (PD-1). We also assess the role of STAT3 in T helper (Th) subtypes cytokine expression.

Food allergy (FA) has emerged as a life-threatening disease worldwide with gastrointestinal damage. The imbalance of intestinal flora and immune response are related to food sensitivities. It is found that the interleukin-33/suppression of tumorigenicity 2 pathway may involve the occurrence and development of allergic diseases. This study aimed to examine the relationships among gut microbiota, immune function, and FA, and evaluate the potential of an oral exposure to Bifidobacterium breve M-16V (Bb M-16V) to relieve allergy symptoms in a mouse model of FA. The results seek to provide a new basis for the application of Bb M-16V in FA and reveal the vital function of different intestinal microbiota composition after exposure to allergen in regulating T cell responses to intestinal allergic reactivity.

Effects of rooibos extract (GRT) and atorvastatin (ATV) treatments on reactive oxygen species (ROS) production in C3A cells without palmitate and cells treated with 500 µM palmitate for 24 hrs. The addition of GRT failed to ameliorate ROS production induced by ATV treatment.

Overall inhibitory effect of miR-506-3p towards receptor activator of nuclear factor kappa B ligand/nuclear factor of activated T cells 1 signaling in bone marrow-derived macrophages.

Protectin conjugates in tissue regeneration 1 (PCTR1) upregulates sodium channel expression via activating the ALX/cAMP/P-Akt/Nedd4-2 pathway and increases Na, K-ATPase expression and activity to promote alveolar fluid clearance. Moreover, PCTR1 also promotes the expression of LYVE-1 to recover the lymphatic drainage resulting in an increase of lung interstitial fluid clearance.

FoxA2 is expressed by hepatic progenitor cells in cirrhotic human liver. FoxA2 suppresses the proliferation of hepatic progenitor cells via reducing glycolysis. FoxA2 inhibits gene transcription, protein expression, and enzyme activities of HK2. FoxA2 reduces PI3K expression and Akt phosphorylation, thus restricting HK2 activity, glycolysis, and proliferation.

Platelet-derived growth factor can induce abnormal proliferation of pulmonary artery smooth muscle cells (PASMCs). Nucleotide-oligomerization domain-like receptor subfamily C3 (NLRC3) suppresses activation of the phosphoinositide 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling thus inhibits PASMCs proliferation. These findings unveiled the effect of NLRC3 as an inhibitor of the PI3K-mTOR pathway mediating protection against PASMCs proliferation.

Tissue expression levels of BDNF and PNKY were correlated with age (p < .0001). Significant inverse correlations were detected between the tissue expression levels of PNKY and both BDNF-AS and MIR137HG (r = −.73, p < .0001 and r = −.43, p < .0001, respectively). Significant pairwise correlations were found between blood levels of BDNF and both BDNF-AS and PNKY, blood levels of MIR137HG, and MIAT as well as tissue levels of BDNF-AS and MIR137HG.

In this study, we found that trophoblast cells constitutively expressed the cytosolic DNA sensors, absent in melanoma 2 (AIM2) and interferon-inducible protein 16 (IFI16). Elevated cell-free fetal DNA might increase the AIM2 and IFI16 activation in women with pre-eclampsia, and elicited increased production of AIM2-mediated IL-8, IL-6 and CCL2 and IFI16-mediated sEndoglin, sFlt-1 and CXCL10, which correlate with the severity of the disease.

Our results indicated that cisplatin-resistant human epidermoid carcinoma KCP-4 cells showed lower β-actin expression and structural disruption of actin filaments, but not its parental KB cells. We here demonstrated that disruption of actin filaments caused dysfunction of volume-sensitive anion channels, which elicits cisplatin resistance in human epidermoid carcinoma cells.

The hominidae-specific histone variant H4G likely forms transient nucleosome-like-structure that undergoes rapid dissociation. Our results suggest that H4G relaxes the nucleolar chromatin and enhances rRNA transcription by forming destabilized nucleosome in breast cancer cells.

In this study, we described our novel finding that the overexpression of Forkhead box C1 promoted Schwann cell migration via the Wnt/β-catenin pathway to improve facial function after nerve crush injury. Our findings may lead to new treatment strategies for facial nerve injury.

Co-NMS could disrupt the mitochondrial function, and subsequently leading to severe impairments in the irradiated glioma cells. Meanwhile, Co-NMS at 5 μM did not induce the apparent neurotoxicity in the zebrafish normal brain.

The proliferation and migration of vascular smooth muscle cells are one of the key regulatory links of atherosclerosis. Our research suggested that smooth muscle and endothelial cell-enriched migration/differentiation-associated lncRNA (SENCR) affects human aortic-VSMCs proliferation and migration via regulating the miR-4731-5p/FOXO3a pathway.

Temporal modulation of calcium sensing in hematopoietic stem cells (HSCs) by store-operated calcium entry (SOCE) inhibitors SKF and 2-aminoethoxydiphenyl borate (2-APB) could be used to expand HSCs ex vivo. Human bone marrow (BM)-HSC and mPB-HSC are highly responsive to modulation of calcium-sensing pathways in comparison with UBC HSCs. SKF and 2-APB significantly increases CFU-GEMM colonies.

We described that homozygous knock-in BDNF Met/Met mice were overweight and hyperphagic compared to wildtype BDNF Val/Val mice. These alterations were associated with gene expression changes of BDNF, SIRT1, and ObR in the hypothalamus and white adipose tissue. Moreover, plasmatic leptin levels were decreased in BDNF Met/Met mice.

The expression of the G-protein-coupled P2Y₆ receptor increases in response to inflammatory stressors. In this study, we have shown that this receptor activity stimulates the formation of key migratory structures to drive cell migration by a dialogue between the Gq/calcium/PKCα and G13/ROCK pathways.

This study showed that trichostatin A (TSA) could rescue impaired osteogenic differentiation of gingiva-derived mesenchymal stem cell (GMSCs) from inflammatory conditions, reduce inflammation, and promote periodontal tissue repair in vivo by inhibiting nuclear factor-κB (NF-κB) signaling. These results indicated that epigenetic modifiers might be a promising therapeutic approach in clinical treatments of periodontitis.

Cosilensing of S1PR1 and GP130 by using small interfering RNA (siRNA)-loaded alginate-conjugated trimethyl chitosan nanoparticles significantly suppresses cancer progression.

• 1.

  MicroRNA-216a-3p (miR-216a-3p) overexpression exerts antitumor effect in cervical cancer.

• 2.

  Knockdown of actin-like 6A (ACTL6A) inhibits the activation of yes-associated protein (YAP).

• 3.

  miR-216a-3p exerts antitumor effect through targeting ACTL6A.

Our results demonstrated that TAM-mediated prostate cancer (PCa) progression is partially attributed to the aberrant expression of miR-95 in TAM-derived exosomes, and the miR-95/JunB axis provides the groundwork for research on tumor-associated macrophages (TAMs) to further develop more-personalized therapeutic approaches for patients with PCa.

In this study, we focused on the effects of in vitro maturation (IVM) on mitochondrial function and Ca²⁺ oscillations in oocytes. We analyzed three groups: in vivo matured oocytes, oocytes matured in vitro with cumulus cells (cumulus oocyte complex [COC] group), and oocytes matured in vitro without cumulus cells (denuded oocyte [DO] group) in our experiments.

This study assesses whether a rapid differentiation could improve the osteogenic potential of the three-dimensionally printed Ti6Al4V (3DTi) scaffolds. The rapid osteoinduction of iPSCs combined with 3DTi scaffolds is a safe, effective, and reproducible method for repairing mandibular bone defects.

We conclude that oxidized and reduced vitamin C are potent antiaging therapies and that DHA reverses the kidney damage observed in SAMP8 mice to a greater degree.

Epidural electrical stimulation (ES) triggers Wnt signaling in the rat thoracic contusion model. ES can activate Wnt/β-catenin signal transduction pathways with contribution of the endocannabinoid system and brain-derived neurotrophic factor (BDNF).

Effective therapeutic strategies are needed to preserve renal function in patients with atherosclerotic renal artery stenosis (ARAS). The current study shows that addition of MSCs improves density of capillaries and microvascular endothelial function in vivo in SW-treated stenotic kidneys, possibly by increasing nitric oxide bioavailability, decreasing renal oxidative stress, and upregulating anti-inflammatory mediators.

CCAT1 increases LXRα transcription by serving as a competing endogenous RNA for miR-613 in an LXRE-dependent manner, thereby promoting lipid droplet formation and nonalcoholic fatty liver disease (NAFLD). CCAT1 and LXRα might be potent targets for NAFLD treatment.

We identified a four immune-related genes (IRGs) signature consisting of four IRGs (CXCL2, SEMA3G, PDGFD, and UCN) through lasso regression and multivariate Cox regression analysis,and this four IRGs signature could effectively predict the prognosis of patients with renal clear cell carcinoma (ccRCC), and its predictive power is independent of other clinical factors. In addition, the correlation analysis of immune cell infiltration showed that this four IRGs signature could effectively reflect the level of immune cell infiltration of ccRCC.

Silencing of microRNA-204-5p (miRNA-204-5p) in C2C12 myotubes enhanced mitochondrial biogenesis, via regulation of PGC-1α. In humans, low expression of miRNA-204-5p in skeletal muscle was associated high oxidative capacity. These findings identify miRNA-204-5p as an interesting modulator of mitochondrial function in human skeletal muscle.

By chelating Fe²⁺, desferoxamine (DFO) was reported to be able to activate the HIF-1α/VEGF pathway and promote angiogenesis. In the present study, we demonstrated that DFO administration could promote angiogenesis and bone repair in glucocorticoid-induced osteonecrosis of the femoral head.

The purpose of the present research was to investigate the protective effects of quercetin on gastrocnemius muscle ischemia-reperfusion.

We found that angiotensin converting enzyme II (ACE2) expression in fibrotic lungs mainly locates in arterial vascular cells, and might provide a route for bloodstream spreading of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Failed human hearts have a higher percentage of ACE2-expressing cardiomyocytes, and SARS-CoV-2 might attack cardiomyocytes through the bloodstream in patients with heart failure. Moreover, ACE2 was highly expressed in cells infected by RSV or Middle East respiratory syndrome coronavirus (MERS-CoV) and in mice treated by lipopolysaccharide (LPS).

A high level of N6-methylation in LncPGCAT-1 can enhance the adsorption capacity of LncPGCAT-1 to gga-mir-1591 for activating the MAPA1/ERK signal to regulate the formation of PGC by relieving the inhibition of MAPK1 expression with gga-mir-1591. Meanwhile, LncPGCAT-1 can interact with ILF3 for regulating the ubiquitination of P53 and phosphorylation of JNK to achieve self-positive feedback regulation of LncPGCAT-1 and activation of the JNK signal, respectively, for promoting the formation of PGC.

We have reported that blocking the degradation of epoxyeicosatrienoic acids (EETs) derived from arachidonic acid could attenuate the lipopolysaccharide-induced acute lung injury (ALI) in mice. The underlying mechanisms remain important questions. Herein, we found that EETs inhibit the activation of nucleotide-binding domain leucine-rich repeat-containing receptor, pyrin domain-containing-3 inflammasome by suppressing calcium overload and reactive oxygen species production in macrophages, contributing to the therapeutic potency to ALI.

The capacity for angiogenesis in endothelial cells could be enhanced by paeoniflorin (PF) treatment via the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) pathway in vitro and could accelerate the wound healing process in vivo through collagen deposition and angiogenesis in regenerated tissue. This study provides evidence that application of PF represents a novel therapeutic approach for the treatment of cutaneous wounds.

Kashin–Beck disease (KBD) is a complex endemic osteoarthropathy. We performed a bioinformatics analysis first to identify the biological mechanisms involved in selenoproteins. The methylation status of iodothyronine deiodinases 3 (DIO3) gene and DIO3 gene expression, as well as DIO3-related regulatory genes in patients with KBD, were analyzed. We found that 15 CpG sites of six selenoproteins were hypomethylated with 5-azacytidine treatment. DIO3 hypermethylation was associated with an increased risk of KBD and may lead to downregulation of DIO3 gene expression as well as be an indicator of the severity of KBD, which may provide a new insight for gene–environment correlations and interactions in etiology and pathogenesis of KBD.

Using Cre-loxP-based approaches, we for the first time demonstrated that tamoxifen-induced Cre-recombinase-mediated downregulation of Pik3c3 expression in renal proximal tubule cells alone is sufficient to significantly inhibit UNX- or amino acid-stimulated mechanistic target of rapamycin complex 1 (mTORC1) signaling to phosphorylation of ribosomal protein S6 (rpS6) and, consequently, prevent UNX- or amino acid-induced hypertrophic nephron growth in adult mice. Our additional cell culture experiments using RNAi confirmed that knocking down Pik3c3 expression inhibits amino acid-stimulated mTORC1–S6K1 signaling activity and blunts cellular growth in the primary cultures of renal proximal tubule cells. Together, both in vivo and in vitro experimental results in the present study indicate that Pik3c3 is a major mechanistic mediator responsible for sensing amino acid availability and initiating hypertrophic growth of renal proximal tubule cells by activation of the mTORC1–S6K1–rpS6 signaling pathway through a mechanism of recruiting mTOR to its activation site—the lysosomal membranes.

Leg ulcer showing, epidermal expression of the inducible arginase isoform (a and b) and its correlation with the epidermal proliferative activity labeled by Ki67 (c). (d, e) Localization of the inducible arginase isoform (green) in proliferating cells (red) in the dermis.

IL-36RN exerted atheroprotective functions through IL-36RN/NLRP3 inflammasome pathway.

Arginase type II (Arg-II) promotes melanoma cell proliferation dependently of its enzymatic activity, while promotes metastasis-related migration and adhesion to endothelial cells through H2O2-STAT3 pathway independently of the enzymatic activity.

Suppressing Arg-II expression rather than inhibiting its enzymatic activity may represent a novel strategy for the treatment of melanoma.

Higher inflammatory factors promote macrophage infiltration and the adipose tissue regeneration process at the donor site. This process is delayed at the recipient site, which may affect long-term retention of fat grafts.

The dipeptidyl peptidase-4 (DPP-4) was identified as a direct and functional target of miR-448-3p in the development of diabetic vascular dysfunction. miR-448-3p alleviated the aortic endothelium damage via inhibited endothelial–mesenchymal transition (EndMT) by degrading DPP-4. Moreover, DPP-4 might regulate EndMT through the transforming growth factor-β/Smad pathway in diabetic endothelial dysfunction.

We demonstrate that suppression of transient receptor potential cation channel subfamily M member 7 (TRPM7) via TRPM7 knockdown or pharmacological inhibition synergistically increases TRAIL-induced antiproliferative effects and apoptosis in triple-negative breast cancer (TNBC) cells. Furthermore, we show that the synergistic interaction might be associated with TRPM7 channel activities using combination treatments of TRAIL and TRPM7 inhibitors (NS8593 as a TRPM7 channel inhibitor and TG100-115 as a TRPM7 kinase inhibitor). We reveal that downregulation of cellular FLICE-inhibitory protein (c-FLIP) via inhibition of Ca²⁺ influx might be involved in the synergistic interaction.

microRNAs (miRNAs) and circular RNAs (circRNAs) are important for endometrial receptivity establishment and embryo implantation in mammals. These results suggest that miR-34a/c not only induce caprine endometrial epithelial cell (CEEC) apoptosis by binding to circ-8073 and CEP55 via the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways, but may also regulate RE establishment in dairy goats.

Coinhibition of cytotoxic T-lymphocyte-associated protein-4 (CTLA-4) and adenosine receptor (A2AR) checkpoint molecules by small interfering RNA (siRNA)-loaded nanoparticles significantly enhances antitumor T-cell responses.

Our findings revealed a novel mechanism that the proinflammatory cytokines IL-1β and TNF-α modulate corneal epithelial wound healing via the p16^Ink4a-p-STAT3 signaling.

Helicobacter pylori (H. pylori) infection of gastric cells results in cagA-dependent activation of the mechanistic target of rapamycin complex 1 (mTORC1), and mTORC1 promoted CCL7, CXCL16, and LL37 production, which might contribute to inflammation and host denfence in H. pylori infection.

Here we present MORPHEUS, a new Fiji/ImageJ2 plugin for the automated evaluation of cell morphometry from images acquired by fluorescence microscopy. The whole algorithm is implemented as a one-click procedure, thus minimizing the user's intervention. By reducing biases and errors of human origin, MORPHEUS is intended to be a useful tool to enhance reproducibility in bioimage analysis