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Cardiac Lipotoxicity: Molecular Pathways and Therapeutic Implications

  • Pathophysiology: Neuroendocrine, Vascular, and Metabolic Factors (SD Katz, Section Editor)
  • Published:
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Abstract

Diabetes and obesity are both associated with lipotoxic cardiomyopathy exclusive of coronary artery disease and hypertension. Lipotoxicities have become a public health concern and are responsible for a significant portion of clinical cardiac disease. These abnormalities may be the result of a toxic metabolic shift to more fatty acid and less glucose oxidation with concomitant accumulation of toxic lipids. Lipids can directly alter cellular structures and activate downstream pathways leading to toxicity. Recent data have implicated fatty acids and fatty acyl coenzyme A, diacylglycerol, and ceramide in cellular lipotoxicity, which may be caused by apoptosis, defective insulin signaling, endoplasmic reticulum stress, activation of protein kinase C, MAPK activation, or modulation of PPARs.

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Funding

Dr. Konstantinos Drosatos is supported by a National Heart, Lung, and Blood Institute (NHLBI) K99/R00 award (1K99HL112853-01). Dr. P. Christian Schulze is supported by a NHLBI K23 award (K23HL24534).

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Konstantinos Drosatos declares that he has no conflict of interest.

P. Christian Schulze declares that he has no conflict of interest.

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Drosatos, K., Schulze, P.C. Cardiac Lipotoxicity: Molecular Pathways and Therapeutic Implications. Curr Heart Fail Rep 10, 109–121 (2013). https://doi.org/10.1007/s11897-013-0133-0

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