Shyam Sundar Nandi
University of Nebraska Medical Center, Indian Institute of Chemical Biology CSIR, University of Burdwan
About
Shyam Nandi, Ph.D., Assistant Professor Research, University of Nebraska Medical Center, USA. Research in the laboratory is focused on the neural regulation of cardiovascular and renal function in health and disease states. We are studying several mechanisms of the mitochondrial dysfunctions in adverse cardiac and renal remodeling during disease states such as heart failure, diabetes, and hypertension. We hypothesized that mitochondrial dysfunction contributes to the exaggerated sympathoexcitation and adverse cardiac and renal remodeling in chronic heart failure. A compromised mitochondrial quality control mechanism (fission-fusion dynamics, biogenesis and mitophagy) contributes to mitochondrial dysfunction in heart failure. Mitochondrial dysfunctional have two-fold effects on cardiac muscle/ cell: a) it reduces ATP generation; b) it increases reactive oxygen species (ROS) generation. Recent clinical trials show that ROS level cannot be scavenged through antioxidant therapy. Therefore, an alternate strategy is required to reduce the levels of ROS generated from mitochondrial dysfunction in heart failure. ROS-producing defective mitochondria can be removed by the process of mitophagy/ autophagy activation. However, mitophagy/ autophagy plays both protective and/or detrimental roles in the heart/cardiomyocytes in a stimulus-dependent manner. The goal of my research is to normalize the altered mitochondrial quality control mechanisms, ROS generation, metabolic shift, and associated mitophagic/ autophagic maladaptations to mitigate the adverse cardiac and renal remodeling in chronic heart failure. My special emphasis is to explore the mechanisms of mitochondrial abnormality in heart failure and its regulation by hypoxia-inducible factor 1-alpha (HIF1A), a master regulator of O2 homeostasis and small molecules (e.g. miRNAs/ lncRNAs) that regulates HIF1A. Manipulation of mitochondrial quality control mechanisms by these molecules will be important and new therapeutic targets for the better management of chronic heart failure. Overall, my research will employ the integrative approach through biochemical, molecular biology, electrophysiological, hemodynamic and renal function measurements, and techniques applied to experimental rodent models of chronic heart failure and in vitro cell cultures.
Employment
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University of Nebraska Medical Center Assistant Professor2021 - Present
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University of Nebraska Medical Center Instructor2018 - 2021
Education
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University of Nebraska Medical Center AHA Postdoctoral Fellow (American Heart Association Award no: 16POST30180003)2016 - 2018
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University of Nebraska Medical Center Postdoctoral Research Associate2013 - 2016
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Indian Institute of Chemical Biology CSIR Ph.D.2007 - 2013
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University of Burdwan MS2003 - 2005
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St. Xavier's College BS2000 - 2003
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Gossner College HS1997 - 1999
Projects & Funding
Projects & funding information is unavailable.
Publications (71)
- Enhanced central sympathetic tone induces heart failure with preserved ejection fraction (HFpEF) in rats. Save
- MMP9 inhibition increases autophagic flux in chronic heart failure Save
- Neurogenic Hypertension Mediated Mitochondrial Abnormality Leads to Cardiomyopathy: Contribution of UPRmt and Norepinephrine-miR-18a-5p-HIF-1a Axis Save
- A Critical Role for the Paraventricular Nucleus of the Hypothalamus in the Regulation of the Volume Reflex in Normal and Various Cardiovascular Disease States. Save
- Enhanced Expression and Function of Renal SGLT2 (Sodium-Glucose Cotransporter 2) in Heart Failure: Role of Renal Nerves Save
- Neurogenic Hypertension Mediated Mitochondrial Abnormality Leads to Cardiomyopathy: Contribution of UPRmt and Norepinephrine-miR- 18a-5p-HIF-1α Axis. Save
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1. Save
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition). Save
- Central Ang II (Angiotensin II)-Mediated Sympathoexcitation Save
- Role of the Renal Nerves in Regulating SGLT2 inhibitor-induced Diuresis and Natriuresis in rats with Heart Failure Save