Jagadeesh Ramasamy

About

Dr. Jagadeesh Ramasamy, PhD, is Director of Bioscience Research–Hematology/Oncology and Associate Professor (Research) at the University of Illinois, and a translational scientist recognized for advancing rigorous, reproducible discovery in red blood cell biology. He first challenged long-standing hematology dogma through his seminal demonstration of mitochondrial persistence in reticulocytes and mature red blood cells (Experimental Hematology, 2017), redefining the understanding of erythrocyte maturation. Building on this foundational discovery, his work established that retained erythrocyte mitochondria drive pathogenic release of mitochondrial DNA, excessive mitochondrial reactive oxygen species, and pro-inflammatory extracellular vesicles, accompanied by dysregulation of selective autophagy proteins including GABARAP, α-synuclein, and cathepsin B (Experimental Hematology, 2025). These mechanisms have broad implications for chronic inflammation and immune-mediated diseases. His current research focuses on developing natural peptide therapeutics to restore mitochondrial homeostasis across diseases. Dr. Ramasamy is a recipient of the NIH Replication Prize-2026 (Track 2: Replication Exemplars).

Employment

• University of Illinois at Chicago Director of Bioscience Research/Associate Professor
  2023 - Present
• University of Illinois at Chicago College of Medicine Research Assistant Professor
  2009 - Present
• University of Chicago Postdoctoral Fellow
  2003 - 2009
• Dana-Farber Cancer Institute Postdoctoral Fellow
  2001 - 2003

Education

• School of Basic Medical Sciences PhD
  1996 - 2001

Projects & Funding

Projects & funding information is unavailable.

Publications (27)

• Mitochondrial retention and autophagy dysregulation drive oxidative stress in sickle cell disease erythrocytes
  Experimental Hematology 2025 DOI: 10.1016/j.exphem.2025.105269
  +Save
• Reticulocyte mitochondrial retention increases reactive oxygen species and oxygen consumption in mouse models of sickle cell disease and phlebotomy-induced anemia.
  Experimental hematology 2023 DOI: 10.1016/j.exphem.2023.02.005
  +Save
• Combinatorial targeting of epigenome-modifying enzymes with small molecule drugs synergistically increases HbF.
  Blood advances 2023 DOI: 10.1182/bloodadvances.2022009558
  +Save
• Oral administration of the LSD1 inhibitor ORY-3001 increases fetal hemoglobin in sickle cell mice and baboons.
  Experimental hematology 2018 DOI: 10.1016/j.exphem.2018.08.003
  +Save
• Pharmacological inhibition of LSD1 and mTOR reduces mitochondrial retention and associated ROS levels in the red blood cells of sickle cell disease
  Experimental Hematology 2017 DOI: 10.1016/j.exphem.2017.02.003
  +Save
• The LSD1 inhibitor RN-1 recapitulates the fetal pattern of hemoglobin synthesis in baboons (P. anubis)
  Haematologica 2016 DOI: 10.3324/haematol.2015.140749
  +Save
• All-trans retinoic acid induces TGF-β<inf>2</inf> in intestinal epithelial cells via RhoA- and p38α MAPK-mediated activation of the transcription factor ATF2
  PLoS ONE 2015 DOI: 10.1371/journal.pone.0134003
  +Save
• RN-1, a potent and selective lysine-specific demethylase 1 inhibitor, increases γ-globin expression, F reticulocytes, and F cells in a sickle cell disease mouse model
  Experimental Hematology 2015 DOI: 10.1016/j.exphem.2015.04.005
  +Save
• Amniotic fluid-borne hepatocyte growth factor protects rat pups against experimental necrotizing enterocolitis
  American Journal of Physiology - Gastrointestinal and Liver Physiology 2014 DOI: 10.1152/ajpgi.00272.2013
  +Save
• Intestinal epithelial apoptosis initiates gut mucosal injury during extracorporeal membrane oxygenation in the newborn piglet
  Laboratory Investigation 2014 DOI: 10.1038/labinvest.2013.149
  +Save