In the past, most studies concerning m6A modification focused on mRNAs. Transcriptome-wide mapping technology reveals a significant presence of m6A-modified lncRNA, which has been shown to play vital roles in biological processes. Interestingly, the expressions and functions of m6A modification are also regulated by lncRNA in turn. The roles of m6A in the regulation of lncRNA mainly concentrate in following aspects: (1) Change the structure of lncRNA and affect its interaction with proteins, known as ‘m6A switch’. (2) Mediate gene transcription repression. (3) Mediate a competing endogenous RNA (ceRNA) model. (4) Regulates lncRNA stability or degradation. However, lncRNA has an impact on m6A regulators as well. LncRNA can influence the stability and degradation of m6A-related enzyme proteins or combine with them to form interaction complexes, thus facilitating a regulatory effect on the downstream target mRNA of m6A regulators. Drug resistance is perhaps the greatest obstacle in improving outcomes for cancer patients, leading to recurrence, progression and metastasis of various cancers. In this review, we summarize all the identified interactions between m6A modification and lncRNA that participate in chemoresistance, aiming to provide a novel insight into the cancer treatment.

Our research investigated the biological roles of CCL2 in NSCLC and discovered that it effectively enhances the migratory and invasive traits of NSCLC cells. Moreover, our findings indicate that CCL2 might promote EMT in NSCLC cells by modulating autophagy and the PI3K/Akt/mTOR signalling pathways.

Under intestinal ischaemia–reperfusion, the activated neutrophils infiltrate the intestine and release NETs. NETs initially bind to Toll-like receptor 4 (TLR4) on the surface of intestinal epithelial cells and further activate the downstream receptor-interacting protein kinase 3 (RIPK3) protein through TLR4. As a protein kinase, RIPK3 impairs FUN14 domain-containing 1 (FUNDC1)-required mitophagy via the phosphorylation of FUNDC1 at Tyr18, which leads to damaged mitochondria in cells that cannot be cleared in time. However, the accumulation of damaged mitochondria results in mitochondrial dysfunction, manifesting as mitochondrial membrane potential loss, ATP synthesis decrease, mt-ROS overproduction, mPTP opening and Cytc leakage. Irreversible mitochondrial dysfunction triggers the mitochondrial-dependent necroptosis pathway and ultimately causes intestinal epithelial cellular necroptosis and gut barrier injury.

This review systematically describes the role of autophagy in macrophage functions, highlighting the existing evidence in the regulation of inflammation, cell death, metabolism, phagocytosis, and so forth. Meanwhile, we summarize the latest progress of therapeutics targeting macrophage autophagy in cardiovascular diseases, hoping to provide novel approaches for future cardiac treatments.

In this study, osteoporotic adipose-derived stem cells (OP-ASCs) were successfully isolated and cultured from the inguinal fat of the OP mouse with bilateral ovariotomy. Lentiviral-mediated overexpression of Wnt10b could enhance the osteogenic ability of OP-ASCs by activating the canonical Wnt signalling pathway to promote the repair of critical-sized calvarial defect in osteoporotic mice.

Nuclear receptor coactive 4 (NCOA4), served as a selective cargo receptor, is critically responsible for the mediation of autophagic degradation of ferritin that is defined as ferrinnophagy. Mechanically, NCOA4-mediated ferritinophagy is considered as a pre-requisite for maintenance of intracellular iron homeostasis by promoting ferritin transport and iron release in accordance with requirements. Therefore, ferritinophagy is of great importance in safeguarding the viability and functionality of cells, and might be a potential therapeutic target for various diseases. In this review, we conclude the latest research findings and regulated mechanisms covering the biological function of NCOA4-mediated ferritinophagy and its contribution to the pathophysiology of ferroptosis. Moreover, the pivotal role of ferritinophagy–ferroptosis axis in human diseases will be discussed in details, proposing to attract attention on the great potential of ferritinophagy in the treatment of various diseases.

Schematic diagram depicting proposed mechanisms of PKM2-induced renal pericyte-myofibroblast transdifferentiation through regulation of transcription levels of downstream LDHA and GLUT1 and lactate production. GLUT1, glucose transporter 1; LDHA, lactate dehydrogenase A; PKM2, pyruvate kinase M2; TGFβ1, transforming growth factor β1.

The schematic pathogenesis of Aβ induced neutrophil neuroinflammation is as follows. Since Aβ interacted with neurons, cellular apoptosis and necrosis initiated. And then mitochondrial DNA (mtDNA) is released from these impaired cells. After being captured by neutrophils, free mtDNA binds to STING protein and activates it. The activated STING protein induces increased expressions of downstream NLRP3 and IL-1β. With released mtDNA, NLRP3 and IL-1β captured by more neutrophils, numerous neutrophils infiltrate into Aβ accumulated regionand aggravate neuroinflammation. This cycle is repeated continuously, which eventually induces neutrophil neuroinflammation and damages neural tissue.

Physical factors influenced both their secretion and, significantly, their biological efficacy. Then, physical factors could also serve as techniques for the engineering of exosomes. The realm of physical factors assumes an instrumental role in modifying and upgrading MSC-Exo, ultimately facilitating their clinical translation.

The biological process of NCs development into NPCs and its cell structure changes.

Overview of the study design and workflow. Single-cell suspensions were collected from BCBrM followed by scRNA-seq on the 10× Genomics platform.

The PI3K/AKT signalling pathway and circadian clock components affect each other in cancer pathologic circumstance resulting in excessive cellular proliferation, apoptosis inhibition, metastasis and resistance to chemotherapy.

Highly aggressive gastric cancer (HAGC) is a gastric cancer characterized by bone marrow metastasis and disseminated intravascular coagulation (DIC), which has a very poor prognosis. Peripheral blood mononuclear cells (PBMCs) were collected from seven HAGC patients, six normal advanced gastric cancer (NAGC) patients, and five healthy individuals for single-cell RNA sequencing using the microwell-seq platform. We identified the cell subpopulations and found that in HAGC patient blood immature neutrophils were greatly increased. Mononuclear phagocytes showed M2-like signatures and T cells were suppressed and reduced in number. Together, they contributed to an immunosuppressive environment in HAGC patients. We also investigated the crosstalk among PBMCs and revealed that intercellular communications were greatly increased in HAGC. Besides, S100A8/A9 and multiple signalling pathways that contribute to DIC were upregulated in HAGC, suggesting their role in HAGC development.

The origin heterogeneity of CAFs: Multiple types of cells, under certain conditions, may become tumour-associated fibroblasts (CAFs). A variety of normal fibroblasts, including resident breast fibroblasts, pancreatic stellate cells (PSCs) and hepatic stellate cells (HSCs), bone marrow-derived mesenchymal stem cells (BM-MSCs) transformed into CAFs under the action of cytokines such as TGF-β. Endothelial cells convert into CAFs through endothelial-mesenchymal transition (EndMT), and epithelial cells differentiate toward CAFs through epithelial mesenchymal-transition (EMT). Adipocytes, pericytes and smooth muscle cells can also be the source of CAFs.

This review can be separated into two sections, one on mechanisms and the other on applications. Acute and chronic wound healing, anti-aging, hair follicle regeneration, and other skincare effects are all supported by the UCMSC secretome in a variety of ways. Different functions in four stages are skin regeneration mechanisms. The review also covers everything from secretome culture, separation, and pretreatment through dosage, administration route, efficacy, and biosafety in the clinic.

TRPV1, a member of the TRP family, is widely expressed in primary sensory neurons and various cells and participates in pain signal transduction of thermal, mechanical and chemical stimulation. Recently, functional changes in TRPV1 channels have been considered as risk factors for OA and RA. Abnormal expression and function of TRPV1 channels are associated with chondrocyte ferroptosis, synovial inflammatory response, macrophage polarization and bone homeostasis. In addition, TRPV1 channels play important roles in neural sensitization, defunctionalization or central sensitization and are involved in the occurrence of pain in OA and RA. Based on clinical and preclinical evidence, TRPV1-targeting drugs and regulation of its expression exhibit prominent curative effects in OA and RA. TRPV1 may be a novel potential therapeutic target for OA and RA treatment.

This review summarises the novel roles of ferroptosis, pyroptosis, and necroptosis in anti-PD-1/PD-L1 immunotherapy. Targeting non-apoptotic regulated cell death in combination with anti-PD1/PD-L1 therapies holds promise as a prospective immunotherapy strategy for tumour treatment.

Schematic diagram for NEK2 functions during porcine embryonic development. NEK2 plays essential roles in normal mitotic division, DNA damage repair and cell cycle progression via the Wnt/β-catenin signalling pathway in porcine early embryogenesis.

In this work, Sun et al. investigated the effect of up-regulation of Gpm6b on the hair cell differentiation of progenitors using Adeno-associated virus-inner ear (AAV-ie)–mediated gene overexpression. In this study, Sun et al. found that Gpm6b overexpression could promote supporting cell proliferation and hair cell differentiation through organoid culture experiments in vivo and viral injection in neonatal mice.

CPPs improve recovery from cardiac injury in mice by their exosomes through the promotion of cardiomyocytic proliferation and vascularization partially by miR-27b-3p mediating the SIK1-CREB1 axis.