Development of hypertrophic cardiomyopathy in perilipin-1 null mice with adipose tissue dysfunction.

@article{Liu2015DevelopmentOH,
  title={Development of hypertrophic cardiomyopathy in perilipin-1 null mice with adipose tissue dysfunction.},
  author={Shangxin Liu and Bin Geng and Liangqiang Zou and Suning Wei and Weiyi Wang and Jingna Deng and Chong En Xu and Xiaojing Zhao and Ying Lyu and Xueying Su and Guoheng Xu},
  journal={Cardiovascular research},
  year={2015},
  volume={105 1},
  pages={20-30}
}
AIMS Perilipin-1 (Plin1), exclusively located on the surface of lipid droplets in adipocytes, regulates the storage and hydrolysis of adipose triglycerides. Plin1 deficiency primarily causes low adiposity and aberrant lipolysis in rodents and humans. Here, we investigated whether adipose tissue dysfunction in perilipin-1 null (Plin1⁻/⁻) mice has maladaptive consequences for the heart and an association with hypertrophic cardiomyopathy. METHODS AND RESULTS Perilipin-1 was expressed… CONTINUE READING

Connections & Topics

Mentioned Connections BETA
Hypertrophic cardiomyopathy in Plin1⁻/⁻ mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans , lipodystrophy and obesity .
Hypertrophic cardiomyopathy in Plin1⁻/⁻ mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans , lipodystrophy and obesity .
Hypertrophic cardiomyopathy in Plin1⁻/⁻ mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans , lipodystrophy and obesity .
Hypertrophic cardiomyopathy in Plin1⁻/⁻ mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans , lipodystrophy and obesity .
Paradoxically , the adipocytes of Plin1⁻/⁻ mice , like those of obese and diabetic mammals , showed robust basal lipolysis and fatty acid efflux to the plasma .
Paradoxically , the adipocytes of Plin1⁻/⁻ mice , like those of obese and diabetic mammals , showed robust basal lipolysis and fatty acid efflux to the plasma .
Excessive fatty acid β-oxidation and lipotoxicity induced excessive production of reactive oxygen species and oxidative stress because antioxidative capacity was reduced in cardiomyocytes , These malefactors injured the myocardial structure and function , as evidenced by disorganized myofilaments as well as irregular and swollen mitochondria with disrupted cristae .
Excessive fatty acid β-oxidation and lipotoxicity induced excessive production of reactive oxygen species and oxidative stress because antioxidative capacity was reduced in cardiomyocytes , These malefactors injured the myocardial structure and function , as evidenced by disorganized myofilaments as well as irregular and swollen mitochondria with disrupted cristae .
Hypertrophic cardiomyopathy in Plin1⁻/⁻ mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans , lipodystrophy and obesity .
Hypertrophic cardiomyopathy in Plin1⁻/⁻ mice with adipose tissue dysfunction may mimic and mechanistically explain the cardiomyopathies occurring in two typical adipose tissue disorders in humans , lipodystrophy and obesity .
All Topics