The Stroop-CN model was developed based on health control results and was used to identify MHE patients among cirrhotic patients. This subset of MHE patients had significantly lower quality of life than non-MHE patients.

1. Immune cell metabolism: Explore the metabolic changes of peripheral immune cells after intracranial aneurysm rupture.
2. Neutrophil heterogeneity: To explore the changes in the composition and function of peripheral blood neutrophils after intracranial aneurysm rupture.
3. Therapeutic insights: Understanding the mechanism of peripheral immune dysfunction in patients after rupture.

To support primary tumor growth, the formation of NETs triggered by tumor-derived CXCL chemokines (CXCL-1, -2, -5, -6, and -8) shield around tumor cells from T cell- and NK-mediated immune attacks. It is possible that these web-like extracellular structures contribute to the robustness of the tumor, leading to the emergence of resistance to immune checkpoint inhibitors. Once in circulation, NETs capture both CTC and CTC/platelet aggregations directly or indirectly by the CCDC25 receptor–ligand interaction, thus facilitating CTC colonization in distant organs. Along with MPO-HOCl, ROS that produced during NETosis impairs lung endothelial barrier integrity and facilitates tumor extravasation by reprogramming the expression of the tight junction protein JAM 1 in the endothelium. More intriguingly, MMP9 and NE located on the NETs can awaken dormant cancer cells by degradation of laminin-111 within ECM.

• Updated review of recent exosomes in liquid biopsy and disease treatment applications

• Recent advances in the use of exosomes as biomarkers in disease applications

• Therapies and efficacy of engineered exosome applications

• Impact of exosomes on precision medicine and personalized treatment

FR15%–Re has long-term negative effects on the host, including abnormal fat accumulation, liver damage, and intestinal inflammation, which are associated with the gut microbiota. ELISA experiments have shown that impaired intestinal barrier function in mice leads to the entry of LPS into the bloodstream and the liver and the downregulation of PPAR-α in the liver.

This study reveals the dose-dependent disease outcomes of SARS-CoV-2 Omicron BA.5 exposure in senescent hamster. High-dose BA.5 exposure results in impaired IFN I signaling, cytokine storm, uncontrolled viral replication, severe lung injury, and death. Early intervention of bio-mimic decoy CoVR-MV rescues critical COVID-19 by viral load inhibition and simultaneous reserving the imbalanced innate immune response from inflammatory to antiviral.

EGFR and TP53 mutations were crucial for early lung cancers development. With EGF/EGFR hypo-methylation accelerating cancer growth by activating EGFR pathway. Transcriptome-based stratification of lung nodules revealed four subtypes (G1-4) related to specific molecular features and immune cell infiltrations. Epigenetic regulation through an array of genes was essential for lung cancer initiation and development.

In this review, we summarize the responsive mechanisms of a variety of endogenous and exogenous stimulus and discuss their biomedical applications, as well as the remaining challenges and outlooks of future research directions for the biomedical applications of stimuli-responsive nanomaterials.

Illustration of CAF^OR-derived CSF2 mediating lnc-CSRNP3 activation in LUAD cells to induce osimertinib resistance. CAF^OR-derived CSF2 was essential for osimertinib resistance by modulating the JAK2/STAT3/lnc-CSRNP3 axis. Lnc-CSRNP3 directly binds to CHD9, promotes CSRNP3 gene expression, and inhibits the phosphatase activity of PP1α, thereby inducing osimertinib resistance by enhancing ribosome biogenesis.

Gut microbiota driving neurological disorders. Gut microbiota may drive neurodevelopmental disorders (ASD and ADHD), neurodegenerative disorders (AD and PD), and mood disorders (anxiety and depression) through gastrointestinal disorders, gut microbiota disorders, decreased diversity of gut microbiota, delayed development of gut microbiota, and so on.

Endothelial dysfunction is commonly linked to various disease states resulting from an imbalance in the production of vasodilators and vasoconstrictors, among other factors. Human diseases associated with endothelial dysfunction include atherosclerosis, diabetes, metabolic syndrome, neurodegenerative diseases, chronic kidney disease, hypertension, heart failure, and stroke.

MenSCs improved serological indices in HBV-Tg mouse model of CCl₄-induced liver fibrosis. The scRNA-seq identified 12 main cell populations in control, CCl₄, and MenSC groups in HBV-Tg mice livers. Reducing ICAM crosstalk between aHSCs and neutrophils is one of the underlying mechanisms. This study highlights interacting target cells and corresponding molecules for MenSCs in treating HBV-associated liver fibrosis.

Bone homeostasis is regulated by complex signaling pathways involving osteoblasts, osteoclasts, and osteocytes, which coordinate bone formation and resorption. Disruption of this signaling network can lead to bone diseases. Additionally, the disease-specific microenvironments in various bone conditions can further disrupt the signaling network and exacerbate disease progression. Consequently, targeting key molecules in these pathways offers promising therapeutic strategies for the treatment of skeletal diseases.

Metabolic disorders seriously endanger the health of human beings. However, there are no approved drugs specific for metabolic disorders. Recently, sever natural products have been demonstrated to alleviate metabolic disorders, and also used as chemical probes to identify their functional targets, which are involved in insulin resistance, glycolipid metabolism, and metabolic inflammation. These developments may facilitate the discovery of natural product-based first-in-class therapeutics against metabolic disorders.

K6 inhibits CRC independent of TP53 by inducing DNA damage and apoptosis, and by downregulating c-Myc to activate PTEN.

Malignant tumor cells regulate pathways such as immune response, angiogenesis, and differentiation of cancer-associated fibroblasts within the tumor microenvironment by recruiting mesenchymal stem cells (MSCs), thereby promoting their own survival and further progression. Leveraging the tumor homing properties of MSCs and the extracellular vesicles (EVs) they secrete, engineered MSCs and EVs are being developed to deliver antitumor substances for precise targeted anticancer therapy.

Diagram of SARS-CoV-2 S protein and HR2-derived lipopeptide fusion inhibitors. The inhibitors IPB24 and IPB28 are designed with a typical flexible linker (PEG4 or GSGSG), whereas the newly designed inhibitor IPB29 uses the amino acid sequence EAAAK as a rigid linker.

The antibodies of ADCs bind to antigens on the cell surface, forming ADC–antigen complexes. These complexes are subsequently internalized into lysosomes via receptor-mediated endocytosis. Once inside the lysosomes, the ADCs can be degraded by enzymes or the acidic environment, releasing cytotoxic payloads that can disrupt DNA or inhibit microtubule polymerization.

This study developed a novel circRNA-based neoantigen vaccine. In vitro experiments showed that circRNA encoding neoantigens can promote DC activation and enhance DC-induced T-cell activation in vitro, thereby enhancing T-cell killing of tumor cells. The circRNA neoantigen vaccine exhibited potent therapeutic and prophylactic effects in diverse murine tumor models by eliciting a robust T-cell-mediated immune response.

Under hypoxia, autophagy is impaired, leading to increased AIM2 protein accumulation. AIM2 promotes M1-type activation of BV2 cells and enhances the expression of ASC, CASP1, and IL-1β, consequently aggravating angiogenesis.

Gene editing is an evolving genetic engineering technology that shows great promise for application in a wide range of human diseases, not only for its therapeutic potential, but also for the construction of animal models of human diseases. This review paper describes the application of gene editing technology in hematological disorders, solid tumors, immune disorders, ophthalmic disorders, and metabolic disorders; highlights the therapeutic strategy of gene editing technology in sickle cell disease; outlines the role of gene editing technology in constructing animal models of human diseases; and discusses the limitations of gene editing technology in the treatment of diseases.

The rapid and orderly process of wound healing depends on the normal function of M1 and M2 and timely phenotypic transformation. However, when M1 phenotype is overexpressed or phenotypic transformation is delayed, it often leads to the pathological healing process of the wound.

Epithelial–mesenchymal plasticity is a crucial mechanism that drive tumor progression, including metastasis, therapeutic resistance, and immune evasion. In this review, we summarized the complicated regulation of EMP and therapeutic strategies targeting EMP for cancer treatment.

Comprehensive summary of therapeutic strategies and corresponding targets in renal cancer.

The graphical abstract showcases the diversity of posttranslational modifications (PTMs) influencing protein structure and function. It features schematic representations of the following 10 prominent PTMs: phosphorylation (addition of phosphate groups), acetylation (addition of acetyl groups), methylation (addition of methyl groups), SUMOylation (attachment of SUMO proteins), ubiquitylation (attachment of ubiquitin molecules), succinylation (addition of succinyl groups), S-nitrosylation (attachment of NO), ADP-ribosylation (addition of ADP-ribose groups), glycosylation (addition of sugar molecules), and palmitoylation (attachment of palmitate groups).

This study has demonstrated that 3-hydroxyphthalic anhydride-modified β-lactoglobulin (3HP-β-LG), a clinically used anti-HPV agent, is effective in inhibiting infection of MPXV, possibly by targeting surface protein A29L of MPXV. Because of its clinically proven safety and stability, 3HP-β-LG shows promise for further development as a prophylactic agent to prevent the sexual transmission of MPXV .

HuProt array is a genome-wide protein array suitable for high throughput unbiased analysis of autoantibodies against the entire human proteome without protein modifications.

We performed RA autoantibody screening in 182 RA patients and 261 controls with HuProt arrays to identify the nonmodified protein antibody profile of RA, especially in ACPA negative patients.

There were five autoantibodies increased in ACPA-negative RA (anti-ANAPC15, anti-LSP1, anti-APBB1, anti-parathymosin, and anti-UBL7). Among them, anti-parathymosin showed the highest prevalence of 46.2% (p = 0.016) in ACPA-negative and early stage (<2years) RA. Prediction model with 44 markers was also constructed with specificity of 90.8%, while the sensitivity is 66.1% (87.8% in ACPA-positive RA patients and 23.8% in ACPA-negative RA).

Ubiquitin-specific protease 22 (USP22) stabilizes SIRT1 and activates the PI3K/Akt/mTOR pathway through enhancing SIRT1-mediated PTEN deacetylation, thereby promoting melanoma metastasis both in vitro and in vivo. Pharmacological or genetic inhibition of USP22 sensitizes ferroptosis by suppressing the PI3K/Akt/mTOR pathway and its downstream target SCD. Furthermore, our study identified topotecan as a clinical USP22-targeting drug capable of effectively suppressing melanoma metastasis in vivo.

We found that low-dose IR can induce RET/PTC1 rearrangement in N-thy-ori-3-1 cell and there is a dose-dependent manner between dose and rearrangement rate. We showed that this progress of IR-induced RET/PTC1 rearrangement requires NHEJ and not HR. Moreover, DNA-PKcs inhibition decreased the repair efficiency of NHEJ. Importantly, the RET/PTC1 rearrangement induced by IR was significantly decreased by DNA-PKcs.

CSR switches IgM to other immunoglobulins. Following immune response or infection within the body, activation of T cell-dependent and T cell-independent antigens triggers the activation of AID, initiating the CSR process. CSR has the capacity to modify the functional properties of antibodies, thereby contributing to the adaptive immune response in the organism.