SAMHITA CHAUDHURI

About

I specifically am working on the downstream regulators of the AKT/m TOR pathway and how it affects cancer. AKT/mTOR pathway is dysregulated and hyperactive in 50–80% of human leukemia cases. AKT hyperactivation correlates with aggressive cancer progression and resistance to a plethora of chemotherapeutics. Targeting The AKT/mTOR pathway could serve as promising strategies for cancer treatment.
Our lab also studies the phenomenon of aging as an intrinsic feature of life. However, aging itself remains the greatest risk factor for all major life-threatening disorders, including Alzheimer's disease, Parkinson's disease, and cardiovascular disease. A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Our lab has a great passion to investigate how mitochondria participate in aging, and to explore effective interventions to counteract aging and aging related diseases. We focus on mitochondrial functions and mitophagy in cardiac physiological and pathophysiological conditions, using novel methodology to quantify in vivo mitophagy and analyze how mitophagy is altered under a host of varying environmental and genetic perturbations. We also seek to elucidate molecular pathways regulating mitophagy using cellular, genetic, and biochemical approaches, as well as genome-scale CRISPR-Cas9 activation/repression screening and high-content image-based chemical screening. The laboratory work ranges from molecular biology to systems physiology using multiple genetically modified mouse models and iPSC technology.

Employment

• Ohio State University Researcher

Education

Education history is unavailable.

Projects & Funding

Projects & funding information is unavailable.

Publications (7)

• Glial Connexin-43 Is a Pathogenic Mechanism Promoting Gut Inflammation in Postoperative Ileus Induced by Gut Surgical Manipulation With Potential Relevance to Humans
  Cellular and Molecular Gastroenterology and Hepatology 2026 DOI: 10.1016/j.jcmgh.2026.101755
  +Save
• USP30 inhibition augments mitophagy to prevent T cell exhaustion
  Science Advances 2025 DOI: 10.1126/sciadv.adv6902
  +Save
• Mitophagy mitigates mitochondrial fatty acid β-oxidation deficient cardiomyopathy
  Nuo Sun, Hayley Barta, Samhita Chaudhuri +16 more
  Nature Communications 2025 DOI: 10.1038/s41467-025-60670-z
  +Save
• BQ788 Reveals Glial ETB R Modulation of Neuronal Cholinergic and Nitrergic Pathways to Inhibit Intestinal Motility: ETB R Signaling is Linked to POI
  British Journal of Pharmacology 2023 DOI: 10.1111/bph.16145
  +Save
• 253c GLIAL CONNEXIN-43 HEMICHANNELS ARE CRITICAL DETERMINANTS OF GUT INFLAMMATION IN MOUSE POSTOPERATIVE ILEUS AND REACTIVE HUMAN ENTERIC GLIA
  Gastroenterology 2023 DOI: 10.1016/s0016-5085(23)04749-2
  +Save
• 472 HIGH-FAT DIET-INDUCED FERROPTOSIS PROMOTES ENTERIC NEURODEGENERATION: A MECHANISM FOR INTESTINAL MOTILITY DISORDERS
  Gastroenterology 2023 DOI: 10.1016/s0016-5085(23)01184-8
  +Save
• Routine patch- clamp recordings in isolated intact neural networks of human myenteric ganglia are a suitable and reliable in vitro technique to study the human little brain in the gut
  Gastroenterology 2022 DOI: 10.1016/s0016-5085(22)60092-1
  +Save