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Glycolysis-Mediated Activation of v-ATPase by Nicotinamide Mononucleotide Ameliorates Lipid-Induced Cardiomyopathy by Repressing the CD36-TLR4 Axis.

Shujin WangYinying HanRuimin LiuMengqian HouDietbert NeumannJun ZhangFang WangYumeng LiXueya ZhaoFrancesco SchianchiChao DaiLi-Zhong LiuMiranda NabbenJan F C GlatzXin WuXifeng LuXi LiJoost J F P Luiken
Published in: Circulation research (2024)
NMN preserves heart function during lipid overload by preventing v-ATPase disassembly.
Keyphrases
  • heart failure
  • fatty acid
  • high glucose
  • toll like receptor
  • diabetic rats
  • inflammatory response
  • endoplasmic reticulum
  • atrial fibrillation
  • mouse model
  • oxidative stress
  • endothelial cells