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Photo GMThe Department is excited to welcome Dr. Girish Melkani as associate professor in the Division of Molecular & Cellular Pathology, effective October 1. 

Dr. Melkani comes to UAB from San Diego State University, where he did his postdoctoral studies, followed by his faculty tenure. His research focuses on disruptions of circadian rhythms associated with cardiometabolic, muscular, and sleep disorders that are hallmarks of many genetic, metabolic, and aging diseases. His lab has been at the forefront of developing and using clinically-relevant genetic models of human systemic metabolic abnormalities, cardiometabolic disease, myopathies, neuropathies, and aging using pathophysiological, cell-molecular, genetics, and nutritional approaches. His lab research findings have been published in high-impact research journals, including Science, Nature Communications, Aging Cell, eLife, Human Molecular Genetics, and PLoS Genetics.

Dr. Melkani brings his well-established research program to UAB, including three funded R01s. His first NIH-NIA R01 grant examines why circadian rhythm disruption leads to elevated risk for cardiometabolic disease/aging and determining how a dietary intervention using time-restricted feeding (TRF) attenuates these risks.

Dr. Melkani's lab also has a long-running interest in understanding the cell-molecular basis of cardiomyopathies and neuropathies linked with protein misfolding/aggregation. In collaboration with Salk Institute, the goal of his second NIH-NIA MPIR01 grant is to investigate the impact of circadian rhythm disruptions in Alzheimer's Disease induced aging in neuronal and peripheral tissues and whether TRF can ameliorate these pathologies.

His third NIH-NHLBI MPIR01 goal is to assess the contribution of insomnia in cardiovascular disease in Drosophila and humans, to delineate biological pathways linking sleep/circadian rhythms with cardiovascular diseases. Recent human GWAS finding, genes linked to sleep disorders in humans, have also led to several loci implicating metabolic processes. His lab is generating fruit-fly models of these risk loci, and exploiting them to identify causal genes, discover mechanistic biology and propose new therapeutic hypotheses that can be extended to humans in collaboration with Massachusetts General Hospital/Harvard.

A complementary focus of Dr. Melkani's research is to understand the genetic and mechanistic basis of cardiomyopathies, skeletal myopathies, and lipodystrophies that arise from mutations of LMNA. His research team has developed Drosophila cardiac and skeletal muscle disease models of laminopathies and validated Drosophila phenotypes in human muscle biopsy tissue from laminopathy patients (recently completed NIH R21 and pending R01 grants). His group is also examining the impact of LMNA mutations on cardiac health in mice. These studies will provide critical insights into treatments for lamin-induced pathologies in humans linked to aggressive, deadly arrhythmias.