NAME: Subir Kumar Roy Chowdhury, MD, PhD

eRA COMMONS USER NAME (credential, e.g., agency login): SUBIRCHOWDHURY

POSITION TITLE: Assistant Research Scientist

EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, include postdoctoral training and residency training if applicable. Add/delete rows as necessary.)

1. Personal Statement

    I am a research scientist specializing in mitochondrial biology, currently focused on understanding the role of mitochondrial metabolism in pediatric critical illnesses. At Nemours Children’s Health, my work investigates mitochondrial dysfunction in pediatric sepsis and diabetic ketoacidosis (DKA), including the development of a cecal slurry mouse model to study both mitochondrial impairment and cognitive outcomes in sepsis survivors.

I have successfully developed and optimized a reporter assay to assess mitochondrial dysfunction in plasma-treated human embryonic kidney (HEK293) cells. In addition, I have mentored NUSRP undergraduate students in adapting this assay for use with human umbilical vein endothelial cells (HUVECs) and in evaluating mitochondrial dysfunction in a septic slurry mouse model. I also collaborate with UC Davis to investigate mitochondrial impairment in children with DKA.

    Throughout my career, I have contributed to research exploring mitochondrial dysfunction in a range of diseases, including diabetic neuropathy, Alzheimer’s disease, chronic lymphocytic leukemia, atherosclerosis, prostate cancer, and various inherited mitochondrial disorders. I have also collaborated with other investigators to support mitochondrial research in diverse areas such as brain tumors, sepsis in canine models, cardiovascular diseases, and rabies virus infection, including training their teams in relevant mitochondrial assays and methodologies.

    My extensive experience in mitochondrial research and ongoing work with septic pediatric populations uniquely positions me to investigate endothelial dysfunction in sepsis and DKA, particularly its role in acute kidney injury (AKI). This work directly supports the Delaware INBRE research vision, advancing our understanding of mitochondrial dysfunction and systemic mediators as drivers of AKI, with strong potential for translational applications.

My present research contributions at Nemours Children’s Health are attributed in the following manuscripts:

1. Khan M, Farooqi S, Mitchell M, Roy Chowdhury SK, Cabrera-Ayala M, Wallace DC, *Weiss SL. Effect of sodium butyrate on kidney and liver mitochondrial dysfunction in a lipopolysaccharide mouse model. FASEB J.2024. Dec 15;38(23):e70228. PMID:39641547 2024.
2. *Weiss SL, Farooqi S, Roy Chowdhury SK, Cabrera-Ayala M, Fernandez L, Chu S, O’Donnell ME, Kuppermann N, Glaser NS. Kidney mitochondrial Complex I dysfunction in a juvenile rat model of diabetic ketoacidosis. Submitted, Pediatric Research, 2025.
3.  

Ongoing projects:

NCHD CRRC (PI: Roy Chowdhury)
07/01/2025 – 06/30/2027
Comparative Analysis of Kidney Mitochondrial Dysfunction in Pediatric Sepsis and Diabetic Ketoacidosis

I have not published or created research products under another name.

Previously funded grants as a principal investigator.

• A two-year postdoctoral grant from the U.S. Army, Department of Defense, USA for the project "Role of mitochondria in prostate cancer". Total amount: 120,000 USD, 2004 - 2006                                                                                          
• A three-year grant from the Grant Agency of Charles University, Prague,

        Czech Republic for the project "The function of mitochondrial glycerophosphate dehydrogenase in production of oxygen radicals". Total amount: 600,000 CZK, 1999 - 2001.                                                                                    

2. Positions, Scientific Appointments, and Honors
    

Positions and Scientific Appointments

2023 - present    Assistant Research Scientist, Nemours Children’s Health, Wilmington, Delaware, USA

2022 - 2023        Senior Research Associate, University of Kansas Medical Center, Kansas City, Kansas, USA                                                

2017 - 2022        Research Associate, John Buhler Research Centre, University of Manitoba, Canada

2007 - 2017        Research Associate, St. Boniface Hospital Research Centre, Winnipeg, Canada         

2006 - 2007        Research Associate, CancerCare Manitoba, University of Manitoba, Winnipeg, Canada

Honors

2018                               Oroboros Academic Travel Award, Innsbruck, Austria

2015                               Grant reviewer of Czech Research Foundation, Prague, Czech Republic

2014                               Grant reviewer of Diabetes UK, London, United Kingdom

2013                               Seahorse Bioscience Travel Award, Novato, CA, USA

2013                               Oroboros Academic Travel Award, Innsbruck, Austria

2012                               The Barrie Hesp Scholarship for Keystone Symposia, Boston, MA, USA

2010                               Travel award, Henry G. Friesen Chair in Endocrine and Metabolic Disorders, Canada

2009                               PNS Fellowship Travel Award from the Peripheral Nerve Society, USA

1997-2002          Postgraduate scholarship, The Ministry of Education, Youth and Sports, Czech Republic, 1^st           Medical Faculty, Charles University, Prague

1991-1997        Scholarship for studies of MD, The Ministry of Education, Youth and Sports, Czech Republic, 1^st Medical Faculty, Charles University, Prague

C.          Contributions to Science

1.    Mitochondrial Dysfunction in Diabetic Neuropathy: Research in this area has provided crucial insights into how mitochondrial dysfunction contributes to the development and progression of diabetic neuropathy. These studies have identified disrupted mitochondrial respiratory function, impaired AMP-activated protein kinase (AMPK) signaling, and altered muscarinic receptor activity as major contributors to neuronal damage. Importantly, therapeutic interventions - such as insulin therapy, AMPK pathway modulation, and muscarinic receptor antagonism - have shown potential in restoring neuronal health in diabetic models.

a.  *Roy Chowdhury SK, Zherebitskaya E, Smith DR, Akude E, Chattopadhyay S, Jolivalt CG, Calcutt NA, Fernyhough P. Mitochondrial respiratory chain dysfunction in dorsal root ganglia of streptozotocin-induced diabetic rats and its correction by insulin treatment. Diabetes, 59 (4), 1082-91, 2010. PMCID: PMC2844817.

b.  Akude E, Zherebitskaya E, Roy Chowdhury SK, Smith DR, Dobrowsky RT, *Fernyhough P. Diminished superoxide generation is associated with respiratory chain dysfunction and changes in the mitochondrial proteome of sensory neurons from diabetic rats. Diabetes, 60 (1), 1082-91, 2011. PMCID: PMC3012184.

c.  *Roy Chowdhury SK, Smith DR, Schopansky J, Saleh A, Gomes S, Akude E, Morrow D, Calcutt NA, Fernyhough P. Impaired AMP-activated protein kinase signaling in dorsal root ganglia neurons is linked to mitochondrial dysfunction and sensory neuropathy in diabetes. Brain, 135(6), 1751-66, 2012. PMCID: PMC3359752.

d.  Calcutt NA, Smith DR, Frizzi K, Sabbir MG, Roy Chowdhury SK, Mixcoatl-Zeoutl T, Saleh A, Muttalib N, Van der Ploeg, Ochoa J, Gopaul A, Tessler L, Wess J, Jolivalt CG, * Fernyhough P. Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy. The Journal of Clinical Investigation (JCI), 127(2):608-622, 2017. PMCID: PMC5272197.

2.    Mitochondrial Metabolism in Alzheimer’s Disease: This body of work emphasizes the central role of mitochondrial function in Alzheimer’s disease (AD). Studies have identified how mitochondrial deficits interact with key AD biomarkers such as apolipoprotein E (ApoE), and how these interactions vary by sex and brain region. This research highlights the therapeutic potential of metabolic interventions like creatine supplementation while also underlining the importance of personalized approaches based on sex-specific responses.

a.  Gabrielli AP, Weidling I, Ranjan A, Wang X, Novikova L, Roy Chowdhury SK, Menta B, Berkowicz A, Wilkins HM, Peterson KR, *Swerdlow RH. Mitochondria profoundly influence apolipoprotein E biology. J Alzheimer’s Dis, 92(2):591-604, 2023. PMID:36776072.

b.  *Djordjevic J, Roy Chowdhury SK, Snow WM, Perez C, Cadonic C, Fernyhough P, *Albensi BC. Early onset of sex-dependent mitochondrial deficits in the cortex of 3xTg Alzheimer's mice. Cells, 9(6):1541, 2020. PMCID: PMC7349170.

c.  *Snow WM, Cadonic C, Cortes-Perez C, Adlimoghaddam A, Roy Chowdhury SK, Thomson E, Anozie A, Bernstein MJ, Gough K, Fernyhough P, Suh M, *Albensi BC. Sex-specific effects of chronic creatine supplementation on hippocampal-mediated spatial cognition in the 3xTg mouse model of Alzheimer's disease. Nutrients, 12(11):3589, 2020. PMCID: PMC7700653.

d.  Djordjevic J, Thomson E, Roy Chowdhury SK, Snow WM, Perez C, Wong TP, Fernyhough P, *Albensi BC. Brain region- and sex-specific alterations in mitochondrial function and NF-κB signaling in the TgCRND8 mouse model of Alzheimer’s disease. Neuroscience, 361:81-92, 2017. PMID: 28802916.

3.    Mitochondrial Function in Cancer: This research investigates the role of mitochondrial respiration in cancer, particularly in chronic lymphocytic leukemia (CLL) and prostate cancer. Studies demonstrate how mitochondrial activity correlates with disease severity and response to therapy, specifically the drug ibrutinib. The findings suggest that targeting mitochondrial bioenergetics could enhance diagnostic accuracy and therapeutic outcomes in cancer treatment.

a.  Roy Chowdhury SK, Bouchard EDJ, Saleh R, Nugent Z, Peltier C, Mejia E, Hou S, McFall C, Squires M, Hewitt D, Davidson L, Shen GX, Johnston JB, Doucette C, Hatch GM, Fernyhough P, Marshal A, Gibson SB, Dawe D, *Banerji V. Mitochondrial respiration correlates with prognostic markers in chronic lymphocytic leukemia and is normalized by ibrutinib treatment. Cancers, 12(3):650, 2020. PMCID: PMC7139649.

b. Roy Chowdhury SK, *Banerji V. Targeting mitochondrial bioenergetics as a therapeutic strategy for chronic lymphocytic leukemia. Oxidative Medicine and Cellular longevity, ID2426712, 2018. PMCID: PMC5851432.

c. Roy Chowdhury SK, Gemin A, *Singh G. High activity of mitochondrial glycerophosphate dehydrogenase and glycerophosphate-dependent ROS generation in prostate cancer cell lines. Biochemical and Biophysical Research Communications (BBRC), 333:1139-1145, 2005. PMID: 15967408.

d.  Roy Chowdhury SK, Raha S, Tarnopolsky MA, *Singh G. Increased expression of mitochondrial glycerophosphate dehydrogenase and antioxidant enzymes in prostate cancer cell lines/cancer. Free Radical Research, 41(10): 1116-1124, 2007. PMID: 17886033.

4. Mitochondrial Function in Cardiovascular Diseases. These studies explore how mitochondrial dysfunction contributes to cardiovascular pathologies, particularly under stress conditions such as chemotherapy (e.g., doxorubicin exposure) or lipid-induced injury. The findings show how oxidative stress and impaired mitochondrial activity in cardiac and endothelial cells can drive cardiovascular damage and suggest potential therapeutic targets to mitigate these effects.

a.  Dhingra R, Margulets V, Roy Chowdhury SK, Thliveris J, Jassal D, Fernyhough P, Dorn G, *Kirshenbaum LA. Bnip3 mediates doxorubicin-induced cardiac myocytes necrosis and mortality through changes in mitochondrial signaling. Proceedings of the National Academy of Sciences (PNAS), 111(51): E5537-44, 2014. PMCID: PMC4280597.

b.  Roy Chowdhury SK, Sangle GV, Xie X, Stelmack GL, Halayko AJ, *Shen GX. Effects of extensively oxidized low-density lipoproteins on mitochondrial function and reactive oxygen species in porcine aortic endothelial cells. American Journal of Physiology (AJP) – Endocrinology and Metabolism, 298 (1), E89-98, 2010. PMID: 19843872.

c.  Sangle GV, Roy Chowdhury SK, Xie X, Stelmack GL, Halayko AJ, *Shen GX. Impairment of mitochondrial respiratory chain activity in aortic endothelial cells induced by glycated LDL. Free Radical Biology and Medicine, 48 (6), 2010. PMID: 20036735.

d.  Xie X, Roy Chowdhury SK, Sangle GV, *Shen GX. Impact of diabetes-associated lipoproteins on oxygen consumption and mitochondrial enzymes in porcine aortic endothelial cells. Acta Biochimica Polonica, 57(4): 393-398, 2010. PMID: 20978632.

5. Mitochondrial Dysfunction in Genetic Disorders. This body of work focuses on mitochondrial dysfunction arising from inherited genetic mutations, particularly those affecting the oxidative phosphorylation (OXPHOS) system. Studies identified mutations in genes like SURF1, linked to Leigh syndrome, and novel nuclear gene mutations affecting ATP synthase. The work contributes to diagnostic and therapeutic approaches in managing inherited mitochondrial disorders.

a.  Roy Chowdhury SK, Drahota Z, Floryk D, Calda P, *Houstek J. Activities of mitochondrial oxidative phosphorylation in cultured amniocytes. Clinica Chimica Acta (CCA), 298(1-2): 157-173, 2000. PMID: 10876012.  

b.  Pecina P, Capkova M, Roy Chowdhury SK, Drahota Z, Dubot A, Vojtiskova A, Hansikova H, Houstkova H, Zeman J, Godinot C, *Houstek J. Functional alteration of cytochrome c oxidase by SURF1 mutations in Leigh syndrome.  Biochimica et Biophysica acta (BBA), 1639(1): 53-63, 2003. PMID: 12943968.

c.  Williams Sion L, Taanman JW, Hansikova H, Houstkova H, Roy Chowdhury SK, Zeman J, *Houstek J. A novel mutation in SURF1 of a patient with cytochrome c oxidase deficient Leigh syndrome causes skipping of exon 8. Molecular Genetics and Metabolism, 73(4): 340-343, 2001. PMID: 11509016.

d.  *Houstek J, Klement P, Floryk D, Antonicka H, Hermanska J, Kalous M, Hansikova H, Houstkova H, Roy Chowdhury SK, Rosipal S, Kmoch S, Stratilova L, Zeman J. A novel deficiency of mitochondrial ATPase of nuclear origin. Human Molecular Genetics, 8(11): 167-174, 1999. PMID: 10484764.

Complete List of Published Work in My Bibliography:

https://www.ncbi.nlm.nih.gov/myncbi/subir%20kumar.roy%20chowdhury.1/bibliography/public/