• 9319 Citations
20022020

Research output per year

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Personal profile

Research interests

My research focuses on the mechanisms of programmed cell death in the heart, which plays a central role in causing heart failure in response to ischemic injury and pressure overload hypertrophy. We have previously characterized the role of two stress induced cell death initiators, Bnip3 and Nix, which are pro-death members of the Bcl2 family of apoptosis regulators, and are induced by cardiac ischemic injury and pressure overload on the heart such as in hypertension, respectively. Bnip3 and Nix target to and permeabilize mitochondria leading to programmed cardiomocyte death. Recently, we have found Bnip3 expression induces autophagy in the mouse heart, which contributes to adverse left ventricular remodeling, due to impaired autophagic flux. We have become interested in defining the role of impaired autophagic flux in cardiomyocyte death. Impaired autophagosome-lysosome fusion and accumulation of autophagic vacuoles is the hallmark of Danon disease, a condition characterized by hypertrophic cardiomyopathy, and caused by mutations in Lamp2 gene, which leads to loss of functional LAMP2 protein. We are characterizing the role of LAMP2 in autophagosome-lysosome fusion and autophagic flux, as a determinant of cardiomyocyte viability in normal cardiac physiology and in response to ischemia-reperfusion injury.

Areas of Clinical Interest

Keywords

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Research Output

Author Correction: High-protein diets increase cardiovascular risk by activating macrophage mTOR to suppress mitophagy (Nature Metabolism, (2020), 2, 1, (110-125), 10.1038/s42255-019-0162-4)

Zhang, X., Sergin, I., Evans, T. D., Jeong, S. J., Rodriguez-Velez, A., Kapoor, D., Chen, S., Song, E., Holloway, K. B., Crowley, J. R., Epelman, S., Weihl, C. C., Diwan, A., Fan, D., Mittendorfer, B., Stitziel, N. O., Schilling, J. D., Lodhi, I. J. & Razani, B., Sep 1 2020, In : Nature Metabolism. 2, 9, p. 991 1 p.

Research output: Contribution to journalComment/debate

Open Access
  • Come Together: Protein Assemblies, Aggregates and the Sarcostat at the Heart of Cardiac Myocyte Homeostasis

    Islam, M., Diwan, A. & Mani, K., Jun 4 2020, In : Frontiers in Physiology. 11, 586.

    Research output: Contribution to journalReview article

    Open Access
  • High-protein diets increase cardiovascular risk by activating macrophage mTOR to suppress mitophagy

    Zhang, X., Sergin, I., Evans, T. D., Jeong, S. J., Rodriguez-Velez, A., Kapoor, D., Chen, S., Song, E., Holloway, K. B., Crowley, J. R., Epelman, S., Weihl, C. C., Diwan, A., Fan, D., Mittendorfer, B., Stitziel, N. O., Schilling, J. D., Lodhi, I. J. & Razani, B., Jan 1 2020, In : Nature Metabolism. 2, 1, p. 110-125 16 p.

    Research output: Contribution to journalArticle

  • 5 Scopus citations

    Lysosome impairment as a trigger for inflammation in obesity: The proof is in the fat.

    Rawnsley, D. R. & Diwan, A., Jun 2020, In : EBioMedicine. 56, 102824.

    Research output: Contribution to journalComment/debate

    Open Access
  • Sensing Protein Quality in Cardiac Myocytes p62 Triggers a Lysosomal Response

    Diwan, A. & Gottlieb, R. A., 2020, (Accepted/In press) In : Circulation research. p. 519-521 3 p.

    Research output: Contribution to journalReview article