Platelet‐derived apoptotic vesicles ameliorate nonalcoholic fatty liver disease by regulating lipid metabolism via apolipoprotein A‐II DOI Creative Commons

Yuhe Jiang,

Yike Liao, Zeying Wang

et al.

Deleted Journal, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 16, 2025

Abstract Nonalcoholic fatty liver disease (NAFLD) encompasses a broad range of conditions, commencing with simple steatosis and progressing to non‐alcoholic steatohepatitis, the possibility further deterioration into fibrosis, cirrhosis, ultimately, hepatocellular carcinoma. Unfortunately, there is currently no approved medication for treating NAFLD‐associated steatosis. This underscores need improved therapeutic approaches that can modulate lipid metabolism halt transition from chronic disease. Our previous studies have demonstrated apoptotic vesicles (apoVs), which are produced during apoptosis, show great potential in regulating homeostasis. However, whether they ameliorate NAFLD unknown. In our research, apoVs derived platelets (PLT‐apoVs) as well mesenchymal stem cells (MSC‐apoVs) were used treat NAFLD. The results showed PLT‐apoVs exhibited superior effects diminishing accumulation induced by high‐fat diet than MSC‐apoVs. Through proteomic analysis, we defined validated apolipoprotein A‐II (APOA2) regulator apoV‐mediated MSC adipogenesis, could be target enhance apoV biomedical field. Owing higher expression APOA2, better pave way apoV‐based therapy

Language: Английский

Treating NASH by targeting peroxisome proliferator-activated receptors DOI Creative Commons
Bart Staels, Laura Butruille, Sven Francque

et al.

Journal of Hepatology, Journal Year: 2023, Volume and Issue: 79(5), P. 1302 - 1316

Published: July 17, 2023

Language: Английский

Citations

44
Role of Insulin Resistance in the Development of Nonalcoholic Fatty Liver Disease in People With Type 2 Diabetes: From Bench to Patient Care DOI Open Access
Juan Patricio Nogueira, Kenneth Cusi

Diabetes Spectrum, Journal Year: 2024, Volume and Issue: 37(1), P. 20 - 28

Published: Feb. 1, 2024

Insulin resistance is implicated in both the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and its progression from steatosis to steatohepatitis, cirrhosis, even hepatocellular carcinoma, which known be more common people with type 2 diabetes. This article reviews role insulin metabolic dysfunction observed obesity, diabetes, atherogenic dyslipidemia, hypertension how it a driver natural history NAFLD by promoting glucotoxicity lipotoxicity. The authors also review genetic environmental factors that stimulate steatohepatitis fibrosis their relationship cardiovascular summarize guidelines supporting treatment diabetes medications reduce resistance, such as pioglitazone or glucagon-like peptide 1 receptor agonists.

Language: Английский

Citations

44
Pharmacologic inhibition of lipogenesis for the treatment of NAFLD DOI Creative Commons
William P. Esler, David E. Cohen

Journal of Hepatology, Journal Year: 2023, Volume and Issue: 80(2), P. 362 - 377

Published: Nov. 15, 2023

Language: Английский

Citations

43
Esculin inhibits hepatic stellate cell activation and CCl4-induced liver fibrosis by activating the Nrf2/GPX4 signaling pathway DOI

Shuoxi Xu,

Yonger Chen,

Jindian Miao

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 128, P. 155465 - 155465

Published: Feb. 17, 2024

Language: Английский

Citations

22
Liver Fibrosis: From Basic Science towards Clinical Progress, Focusing on the Central Role of Hepatic Stellate Cells DOI Open Access
Hikmet Akkız, Robert K. Gieseler, Ali Canbay

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(14), P. 7873 - 7873

Published: July 18, 2024

The burden of chronic liver disease is globally increasing at an alarming rate. Chronic injury leads to inflammation and fibrosis (LF) as critical determinants long-term outcomes such cirrhosis, cancer, mortality. LF a wound-healing process characterized by excessive deposition extracellular matrix (ECM) proteins due the activation hepatic stellate cells (HSCs). In healthy liver, quiescent HSCs metabolize store retinoids. Upon fibrogenic activation, transdifferentiate into myofibroblasts; lose their vitamin A; upregulate α-smooth muscle actin; produce proinflammatory soluble mediators, collagens, inhibitors ECM degradation. Activated are main effector during fibrogenesis. addition, accumulation profibrogenic macrophages in response hepatocyte death play role initiation HSC survival. source myofibroblasts resident HSCs. migrate site active fibrogenesis initiate formation fibrous scar. Single-cell technologies revealed that highly homogenous, while activated HSCs/myofibroblasts much more heterogeneous. complex results from various hepatocellular inflammatory signals related intrahepatic pathways or extrahepatic mediators. Inflammatory processes modulate activating and, turn, drive immune mechanisms via cytokines chemokines. Increasing evidence also suggests cellular stress responses contribute Recent data demonstrated can revert even advanced stages cirrhosis if underlying cause eliminated, which inhibits cells. However, despite numerous clinical studies on plausible drug candidates, approved antifibrotic therapy still remains elusive. This state-of-the-art review presents molecular involved its resolution, well comprehensively discusses drivers linking LF.

Language: Английский

Citations

17
Hexokinase 2-mediated metabolic stress and inflammation burden of liver macrophages via histone lactylation in MASLD DOI Creative Commons
Jinyang Li, Xiancheng Chen, Shiyu Song

et al.

Cell Reports, Journal Year: 2025, Volume and Issue: 44(3), P. 115350 - 115350

Published: Feb. 25, 2025

Language: Английский

Citations

2
Hepatic Fibrosis and Cancer: The Silent Threats of Metabolic Syndrome DOI Creative Commons
Scott L. Friedman

Diabetes & Metabolism Journal, Journal Year: 2024, Volume and Issue: 48(2), P. 161 - 169

Published: Jan. 26, 2024

Metabolic dysfunction-associated steatotic (fatty) liver disease (MASLD), previously termed non-alcoholic fatty disease, is a worldwide epidemic that can lead to hepatic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The typically component of the metabolic syndrome accompanies obesity, often overlooked because manifestations are clinically silent until late-stage present (i.e., cirrhosis). Moreover, Asian populations, including Koreans, have higher fraction patients who lean, yet their illness has same prognosis or worse than those obese. Nonetheless, ongoing injury inflammation ballooning hepatocytes as classic features. Over time, fibrosis develops following activation stellate cells, liver’s main fibrogenic cell type. usually more advanced in with type 2 diabetes mellitus, indicating all diabetic should be screened for disease. Although there been substantial progress clarifying pathways no approved therapies yet, but current research seeks uncover driving hopes identifying new therapeutic targets. Emerging molecular methods, especially single sequencing technologies, revolutionizing our ability clarify mechanisms underlying MASLD-associated HCC.

Language: Английский

Citations

14
Resmetirom's approval: Highlighting the need for comprehensive approaches in NASH therapeutics DOI
Salah Abdalrazak Alshehade

Clinics and Research in Hepatology and Gastroenterology, Journal Year: 2024, Volume and Issue: 48(7), P. 102377 - 102377

Published: May 19, 2024

Language: Английский

Citations

13
Myocardial infarction accelerates the progression of MASH by triggering immunoinflammatory response and induction of periosti DOI
Xie Wei, Jing Gan, Xiaodong Zhou

et al.

Cell Metabolism, Journal Year: 2024, Volume and Issue: 36(6), P. 1269 - 1286.e9

Published: June 1, 2024

Language: Английский

Citations

13
Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials DOI Creative Commons
Xingpeng Di, Jiawei Chen, Ya Li

et al.

Clinical and Translational Medicine, Journal Year: 2024, Volume and Issue: 14(1)

Published: Jan. 1, 2024

Abstract Background The impact of fibroblasts on the immune system provides insight into function fibroblasts. In various tissue microenvironments, multiple fibroblast subtypes interact with immunocytes by secreting growth factors, cytokines, and chemokines, leading to wound healing, fibrosis, escape cancer surveillance. However, specific mechanisms involved in fibroblast‐immunocyte interaction network have not yet been fully elucidated. Main body conclusion Therefore, we systematically reviewed molecular interactions from history cellular evolution cell subtype divisions regulatory networks between immunocytes. We also discuss how these communications different organ statuses, as well potential therapies targeting reciprocal interplay fibrosis. A comprehensive understanding functional cells under pathophysiological conditions which they communicate may lead development effective

Language: Английский

Citations

12