promotes liver sinusoidal endothelial cell dysfunction and induces macrophage M1 polarization in non-alcoholic fatty liver disease.

Background: The progression of non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH) and liver fibrosis remains poorly understood, though liver sinusoidal endothelial cells (LSECs) are thought to play a central role in disease pathogenesis.

Aim: To investigate the role of in NAFLD fibrosis through its regulation of LSEC dysfunction and macrophage polarization.

Methods: We analysed single-cell transcriptomic data (GSE129516) from NASH and normal mouse models and identified as a key regulator in LSECs.

CuSO protects hepatocytes from lipotoxicity by promoting autophagic degradation of lipid droplets to attenuate oxidative stress.

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is a prevalent chronic liver condition that often progresses to Metabolic Dysfunction-Associated Steatohepatitis (MASH), ultimately leading to liver fibrosis and hepatocellular carcinoma (HCC). Consequently, the early diagnosis and treatment of MASLD are particularly crucial. Currently, the pathogenic mechanisms underlying MASLD remain incompletely understood, and there is no optimal therapy available for this condition.

Red blood cell-derived extracellular vesicles deliver NUP85 siRNA to alleviate MASLD through downregulating SLC27A1/PPAR-γ in hepatocyte.

Hepatic steatosis and inflammation, resulting from excessive hepatic lipid deposition, are hallmarks of metabolic dysfunction-associated fatty liver disease (MASLD). Recent studies have indicated that nucleoporin 85 (NUP85) influences lipid metabolism in liver cells; however, the role of NUP85 in the diagnosis and treatment of MASLD remains unclear. Firstly, results showed that compared to healthy controls, serum levels of NUP85 were elevated in patients with metabolic dysfunction-associated steatohepatitis (MASH) and cirrhosis, with AUROC values of 0.

Ribosome biogenesis: A central player in liver diseases.

Ribosome biogenesis is a multi-step process that initiates within the nucleolus, terminates in the cytoplasm, and determines the rate of protein synthesis. Ribosome biogenesis is essential for maintaining liver function. In eukaryotes, it involves producing and assembling approximately 200 factors and 80 ribosomal proteins.

promotes lipid metabolism in hepatocellular carcinoma by regulating the signaling pathway through .

Objectives: Cancer cells exhibit altered metabolic profiles. Glutaminase 1 (), a key enzyme in cancer cells, promoting glutamine catabolism to glutamate and ammonia, is strongly associated with various human malignancies.

Methods: promotes lipid accumulation and cell proliferation by upregulating the expression of sterol regulatory element-binding protein 1 () and SREBP cleavage-activating protein ().

Prognostic role of IL-34 in sepsis and sepsis-induced acute lung injury: preliminary results and future directions.

Objective: This study aimed to evaluate the potential of interleukin-34 (IL-34) as a novel biomarker for predicting mortality in sepsis patients, with a specific focus on those with sepsis-induced acute lung injury (ALI).

Methods: This prospective cohort study enrolled 115 sepsis patients admitted to the intensive care unit (ICU). The patients were divided into survival and non-survival groups, as well as ALI and non-ALI subgroups.

Mesenchymal stem cell-derived exosomes as a plausible immunomodulatory therapeutic tool for inflammatory diseases.

Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs), especially, exosomes are considered to have diverse therapeutic effects for various significant diseases. MSC-derived exosomes (MSCex) offer substantial advantages over MSCs due to their long-term preservation, stability, absence of nuclei and fewer adverse effects such as infusion toxicity, thereby paving the way towards regenerative medicine and cell-free therapeutics. These exosomes harbor several cellular contents such as DNA, RNA, lipids, metabolites, and proteins, facilitating drug delivery and intercellular communication.

Mesenchymal stem cell-derived small extracellular vesicles reduced hepatic lipid accumulation in MASLD by suppressing mitochondrial fission.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic liver disease characterized by lipid accumulation in liver cells. Human umbilical cord mesenchymal stem cell-derived small extracellular vesicles (MSC-sEV) have great potential in repairing and regenerating liver diseases. However, it is still unclear whether MSC-sEV can inhibit hepatocyte lipid accumulation by regulating mitochondrial fission.

LIMA1 O-GlcNAcylation Promotes Hepatic Lipid Deposition through Inducing β-catenin-Regulated FASn Expression in Metabolic Dysfunction-Associated Steatotic Liver Disease.

Hepatic lipid deposition is a key factor in progressing metabolic dysfunction-associated steatotic liver disease (MASLD). This study investigates the impact of the LIM domain and actin-binding protein 1 (LIMA1) on hepatic steatotic in MASLD and explore the underlying mechanisms. Increased levels of LIMA1 is observed in both serum and serum sEV of metabolic dysfunction-associated steatohepatitis (MASH) patients compared to healthy controls, with AUROC values of 0.

Microscopic messengers: microbiota-derived bacterial extracellular vesicles in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a persistent and complex condition accomplished by inflammation of the gastrointestinal system, encompassing Crohn's disease (CD) and ulcerative colitis (UC). This condition is caused by the combination of genetic predispositions, environmental triggers, and dysregulated immunological responses, which complicates diagnosis and treatment. The latest developments in gastroenterology have revealed the critical significance of the gut microbiota in the pathogenesis of IBD.

USP9X-enriched MSC-sEV inhibits LSEC angiogenesis in MASH mice by downregulating the IκBα/NF-κB/Ang-2 pathway.

Pathological angiogenesis of liver sinusoidal endothelial cells (LSEC) plays a crucial role in the progression of metabolic dysfunction-associated steatohepatitis (MASH)-induced liver fibrosis. Mesenchymal stem cell-derived small extracellular vesicles (MSC-sEV) have shown promising therapeutic potential against MASH. This study aimed to investigate the impact of MSC-sEV on LSEC angiogenesis and elucidate the underlying molecular mechanisms.

The role of hepatocyte-derived extracellular vesicles in liver and extrahepatic diseases.

Extracellular vesicles (EVs) are vesicle-like bodies with a double membrane structure that are released from the cell membrane or secreted by cells into the extracellular environment. These include exosomes, microvesicles, and apoptotic bodies. There is growing evidence indicating that the composition of liver cell contents changes following injury.

Focus on cuproptosis: Exploring new mechanisms and therapeutic application prospects of cuproptosis regulation.

Cuproptosis is a novel form of regulated cell death, which plays an important role in the physiological and pathological processes of the human body. Despite the increasing research on cuproptosis-related genes (CRGs) and their correlation with diseases, the pathogenesis of cuproptosis-related diseases remains unclear. Furthermore, there is a lack of reviews on the emerging technologies for regulating cuproptosis in disease treatment.

MiR-4465-modified mesenchymal stem cell-derived small extracellular vesicles inhibit liver fibrosis development via targeting LOXL2 expression.

Liver fibrosis is a significant health burden, marked by the consistent deposition of collagen. Unfortunately, the currently available treatment approaches for this condition are far from optimal. Lysyl oxidase-like protein 2 (LOXL2) secreted by hepatic stellate cells (HSCs) is a crucial player in the cross-linking of matrix collagen and is a significant target for treating liver fibrosis.

Lipotoxic hepatocyte derived LIMA1 enriched small extracellular vesicles promote hepatic stellate cells activation via inhibiting mitophagy.

Background: Hepatic stellate cells (HSCs) play a crucial role in the development of fibrosis in non-alcoholic fatty liver disease (NAFLD). Small extracellular vesicles (sEV) act as mediators for intercellular information transfer, delivering various fibrotic factors that impact the function of HSCs in liver fibrosis. In this study, we investigated the role of lipotoxic hepatocyte derived sEV (LTH-sEV) in HSCs activation and its intrinsic mechanisms.

RNF31 alleviates liver steatosis by promoting p53/BNIP3-related mitophagy in hepatocytes.

Background & Aims: Non-alcoholic fatty liver disease (NAFLD) is one of the liver illnesses that may be affected by mitophagy, which is the selective removal of damaged mitochondria. RNF31, an E3 ubiquitin ligase, is carcinogenic in many malignancies. However, the influence of RNF31 on mitochondrial homeostasis and NAFLD development remains unknown.

Immune-related long noncoding RNA zinc finger protein 710-AS1-201 promotes the metastasis and invasion of gastric cancer cells.

Background: Gastric cancer (GC) is a prevalent malignant tumor of the gastrointestinal system. ZNF710 is a transcription factor (TF), and zinc finger protein 710 (ZNF710)-AS1-201 is an immune-related long noncoding RNA (lncRNA) that is upregulated in GC cells.

Aim: To assess the correlation between ZNF710-AS1-201 and immune microenvironment features and to investigate the roles of ZNF710-AS1-201 in the invasion and metastasis processes of GC cells.

Exosomal circRNA: emerging insights into cancer progression and clinical application potential.

Exosomal circRNA serves a novel genetic information molecule, facilitating communication between tumor cells and microenvironmental cells, such as immune cells, fibroblasts, and other components, thereby regulating critical aspects of cancer progression including immune escape, tumor angiogenesis, metabolism, drug resistance, proliferation and metastasis. Interestingly, microenvironment cells have new findings in influencing tumor progression and immune escape mediated by the release of exosomal circRNA. Given the intrinsic stability, abundance, and broad distribution of exosomal circRNAs, they represent excellent diagnostic and prognostic biomarkers for liquid biopsy.

Mesenchymal stem cell-derived exosomal miR-27b-3p alleviates liver fibrosis via downregulating YAP/LOXL2 pathway.

Lysyl oxidase-like 2 (LOXL2) is an extracellular copper-dependent enzyme that plays a central role in fibrosis by catalyzing the crosslinking and deposition of collagen. Therapeutic LOXL2 inhibition has been shown to suppress liver fibrosis progression and promote its reversal. This study investigates the efficacy and underlying mechanisms of human umbilical cord-derived exosomes (MSC-ex) in LOXL2 inhibition of liver fibrosis.

Human umbilical cord mesenchymal stem cell-derived exosomes ameliorate liver steatosis by promoting fatty acid oxidation and reducing fatty acid synthesis.

Background & Aims: Non-alcoholic fatty liver disease (NAFLD) affects nearly a quarter of the population with no approved pharmacological therapy. Liver steatosis is a primary characteristic of NAFLD. Recent studies suggest that human umbilical cord mesenchymal stem cell-derived exosomes (MSC-ex) may provide a promising strategy for treating liver injury; however, the role and underlying mechanisms of MSC-ex in steatosis are not fully understood.

Therapeutic Potential of Extracellular Vesicles from Different Stem Cells in Chronic Wound Healing.

Wound healing has long been a complex problem, especially in chronic wounds. Although debridement, skin grafting, and antimicrobial dressings have been used to treat chronic wounds, their treatment period is long, expensive, and has specific rejection reactions. The poor treatment results of traditional methods have caused psychological stress to patients and a substantial economic burden to society.

hucMSC-Ex Alleviates IBD-Associated Intestinal Fibrosis by Inhibiting ERK Phosphorylation in Intestinal Fibroblasts.

Background: Intestinal fibrosis, one of the complications of inflammatory bowel disease (IBD), is associated with fistula and intestinal stricture formation. There are currently no treatments for fibrosis. Mesenchymal stem cell-derived exosomes have been proven to exert inhibitory and reversal effects in IBD and other organ fibrosis.