Cardiolipin remodeling by ALCAT1 links oxidative stress and mitochondrial dysfunction to obesity.

@article{Li2010CardiolipinRB,
  title={Cardiolipin remodeling by ALCAT1 links oxidative stress and mitochondrial dysfunction to obesity.},
  author={Jia Li and C. Romestaing and Xianlin Han and Yuan Li and Xinbao Hao and Y. Wu and Chao Sun and Xiaolei Liu and L. S. Jefferson and Jingwei Xiong and K. Lanoue and Z. Chang and C. Lynch and Huayan Wang and Yuguang Shi},
  journal={Cell metabolism},
  year={2010},
  volume={12 2},
  pages={
          154-65
        }
}
Oxidative stress causes mitochondrial dysfunction and metabolic complications through unknown mechanisms. Cardiolipin (CL) is a key mitochondrial phospholipid required for oxidative phosphorylation. Oxidative damage to CL from pathological remodeling is implicated in the etiology of mitochondrial dysfunction commonly associated with diabetes, obesity, and other metabolic diseases. Here, we show that ALCAT1, a lyso-CL acyltransferase upregulated by oxidative stress and diet-induced obesity (DIO… Expand

Paper Mentions

Interventional Clinical Trial
The purpose of this study is to provide information regarding potential factors underlying metabolic dysfunction, insulin resistance, and loss of muscle mass in aging muscle.  
ConditionsInsulin Resistance, Sarcopenia
InterventionBehavioral
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TLDR
A key role is reported of ALCAT1, a lysocardiolipin acyltransferase that catalyzes the synthesis of CL with a high peroxidation index, in mitochondrial dysfunction associated with hypertrophic cardiomyopathy, which implicate a key role of A LCAT1 as the missing link between oxidative stress and mitochondrial dysfunction in the etiology of age-related heart diseases. Expand
Cardiolipin remodeling by ALCAT1 links mitochondrial dysfunction to Parkinson’s diseases
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Lysocardiolipin acyltransferase 1 (ALCAT1) controls mitochondrial DNA fidelity and biogenesis through modulation of MFN2 expression
TLDR
An unexpected role of CL remodeling in mitochondrial biogenesis is revealed, linking oxidative stress by ALCAT1 to mitochondrial fusion defect and mtDNA instability and depletion that are reminiscent of MFN2 deficiency. Expand
Mitochondrial bioenergetics and cardiolipin alterations in myocardial ischemia-reperfusion injury: implications for pharmacological cardioprotection.
TLDR
The role played by CL alterations in mitochondria-specific phospholipid alterations in mitochondrial dysfunction in myocardial I/R injury is focused on and pharmacological strategies to prevent myocardIAL injury during I-R targeting mitochondrial CL are examined. Expand
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