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

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

Citations

1