Michael Schlame, MD

  • Specialties: Cardiac Anesthesiology, Anesthesiology
  • Language: English
  • Phone: 212-263-5072
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  • Professor, Department of Anesthesiology, Perioperative Care, and Pain Medicine
  • Professor, Department of Cell Biology
  • Director, Cardiothoracic Anesthesia
Board Certifications
  • American Board of Anesthesiology - Anesthesiology, 2006
Education and Training
  • Residency, NYU Medical Center, Anesthesiology, 2004
  • Residency, New York Presbyterian - Weill Cornell Medical Center, Anesthesiology, 2001
  • MD from Medical Academy Of Magdeburg, 1985

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NYU Anesthesia Associates

550 1st Avenue, Suite 605
New York, NY 10016

Research My Research


cardiomyopathy, lipid biochemistry, mitochondria

Research Summary

Barth syndrome is a hereditary cardiomyopathy that also affects skeletal muscles, growth, and neutrophils. The mutated gene (tafazzin) is homologous to a conserved family of phospholipid acyltransferases. Children with Barth syndrome are deficient in the mitochondrial phospholipid cardiolipin, suggesting that the primary defect of the disease may indeed be found in phospholipid metabolism and may specifically affect the phospholipids of mitochondria. We want to study the mechanism by which tafazzin mutation causes cardiomyopathy and skeletal muscle disease. First, we want to identify the enzymatic function of tafazzin. We will identify the intracellular localization of tafazzin, its impact on lipid composition, and its mechanism of action. Second, we want to examine the effect of tafazzin on structure and function of mitochondria. Since mitochondrial dysfunction is a plausible etiology of cardiomyopathy and skeletal muscle weakness, we will analyze mitochondrial ultrastructure and oxidative phosphorylation in cell lines with tafazzin deletion. Third, we want to explore a Drosophila model of Barth syndrome, which was created in our laboratory. We will study lipid metabolism, muscle physiology, morphology, and mitochondrial ultrastructure in fruit flies with tafazzin deletion. The Drosophila model will also be used for cardiac studies since flies contain a contractile fluid pumping organ that shares conserved features of cardiogenesis with all heart-forming creatures, including humans. The project will provide insight into the pathologic mechanism of a unique disease, which presents a novel pathway from lipid defect(s) to cardio-skeletal myopathy. Such information may be useful for the development of new therapeutic approaches to cardiomyopathy and skeletal muscle disease.

Academic Contact

Academic office

560 First Avenue

Fifth Floor

New York, NY 10016



Research Interests Timeline

These focus areas and their associated publications are derived from PubMed and the MeSH term library.
represents one publication


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