Sanjana Sood

Researcher

University of Arkansas for Medical Sciences

faculty

6 h-index 15 pubs 441 cited

Research Areas

Mitochondrial Function and Pathology Cancer-related molecular mechanisms research Metabolism and Genetic Disorders Birth, Development, and Health Molecular Biology Techniques and Applications Maternal and Perinatal Health Interventions Cancer Treatment and Pharmacology Cardiovascular Function and Risk Factors

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OverviewAI-generated summary

Sanjana Sood's research investigates cellular mechanisms underlying various biological processes, with a focus on cell death, homeostasis, and signaling pathways. Her recent work explores the role of mitochondria in regulating non-apoptotic cell death in cancer, and how thienopyrimidine derivatives can induce mitochondrial dysfunction and mitophagy in triple-negative breast cancer. Sood also studies the modulation of cellular aging and its impact on integrated stress response signaling in controlling blood cell homeostasis. In a separate line of inquiry, her research has examined novel biomarkers for preterm brain injury using the blood transcriptome in a sheep model of intrauterine asphyxia. Her scholarship metrics include an h-index of 6, with 15 total publications and 441 citations.

Metrics

  • h-index: 6
  • Publications: 15
  • Citations: 441

Selected Publications

  • The hidden hand of endoplasmic reticulum stress in anticancer drug resistance (2025) DOI
  • Thienopyrimidine derivatives TPH104c and TPH104m induce JNK/BNIP3-mediated mitochondrial dysfunction and promotes mitophagy in triple-negative breast cancer (2025) DOI
  • Mitochondria as Regulators of Nonapoptotic Cell Death in Cancer (2025) DOI
  • Genetic perturbation of cellular homeostasis regulates integrated stress response signaling to control <i>Drosophila</i> hematopoiesis (2025) DOI
  • Intellectual Property Rights in Neuroprotective Biomaterials (2025) DOI
  • Modulation of cellular ageing regulates Integrated Stress Response signalling to control blood cell homeostasis (2025) DOI

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