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Title : Dr.
First Name : DIVYA
Last Name : BHATIA
University/Institution : Weill Cornell Medicine
Email ID : dib2020@med.cornell.edu
City : New York
Country : United States
State : New york
Zipcode : 10065
Department : Medicine
Company Name :
Area of Research
Kidney diseases, Immunology
Area of Expertise
Autophagy, Fibrosis, Macrophage, Mitophagy, T cells, B cells, Chronic kidney disease
Brief Description of Research Interest :

My research interests include the comprehensive understanding of the molecular mechanism and the function(s) of the mitophagy in modulating immune cell-derived progression of kidney fibrosis, and their role in the transition of acute kidney injury to chronic kidney disease (CKD). My current research at Weill Cornell Medicine is focused on studying the role of mitochondrial autophagy in the modulation of macrophage-induced pro-fibrotic response in progressive CKD. The manipulation of mitophagy’s signaling pathways can be of clinical benefits and helpful for the patients in the prevention of progression of chronic kidney disease. I have been invited asa speaker two years in a row by the American Society of Nephrology in the Kidney Week-2017 and 2018 meetings. My research profile was also highlighted in the brochure of 2nd annual Weill Department of Medicine research retreat. The related manuscript is under consideration by the Journal ofClinical Investigation. I have published 10 papers and at least 15abstracts in peer-reviewed journals.

I completed my doctoral research, which was funded partly by theBritish Council and Indian Council of Medical Research from the prestigious medical school (AIIMS, New Delhi) from India. I looked at the effect ofrituximab on lymphocyte subsets and urinary protein CD80 in patients withsteroid-dependent nephrotic syndrome. The same research was featured on the cover page of “Pediatric Research” (Vol. 84, Issue 4,  October 2018). I also received travel grant and invited as a speaker by the International Pediatric Nephrology Association to present this work in the IPNA-2016 congress. We confirmed an increase in the circulating Th17, Th2, and memory B cells and urinary CD80 excretion during active nephrotic syndrome and their reversal after administration of rituximab. During my Ph.D, I have also contributed to several other projects focused on studying the factors responsible for factor Hand CD46 mutations in patients with the hemolytic uremic syndrome (see publications). During my Ph.D., I was awarded the fellowship by the Faculty of Medicine and Dentistry, Renal Academic Unit of the University of Bristol,United Kingdom. I worked with a group who obtained the patent on human podocyte cell line and studied the effect of Th17 derived cytokines on podocyte cytoskeleton stability. The findings were presented in the UK-Kidney week (Liverpool) in2017 (see related abstract).

To improve my scientific knowledge, I regularly review manuscripts for several journals including AgingScientific ReportsFrontiersin Medicine, American Journal of Nephrology, and PeerJ. I have reviewed at least 30 manuscripts (www.publons.com/researcher/1512241/divya-bhatia/).

Representative Publications :

1. Bharati J, Bhatia D, Khandelwal P, Gupta N, Sinha A, Khadgawat R, Hari P,Bagga A. C-Terminal Fibroblast Growth Factor-23 Levels in Non-Nutritional Hypophosphatemic Rickets. The Indian J Pediatr. Mar 5, 2019.

2. Akchurin O, Patino P, Dalal V, Meza K, Bhatia D, Brovender S, Zhu YS, RundlesSC, Perelstein E, Kumar J, Rivella S, Choi ME. Interleukin-6 contributes to thedevelopment of anemia in juvenile chronic kidney disease. KidneyInternational Rep. Dec. 2018.

3. Pabon M, PatinoE, Bhatia D, Quintero JR, Ma K, Finkelsztein E, Osorio J, MalickF, Polverino F, Owen C, Ryter SW, Choi AMK, Cloonan S, Choi ME. Beclin-1 Regulates Cigarette Smoke-Induced Kidney Injury in a Murine Model of Chronic Obstructive Pulmonary disease. JCI Insight.August, 2018.

4.  Bhatia D,SinhaA, Hari P, Sopory S, Saini S, Puraswani M, Sani H, Mitra DK, Bagga A. Rituximab modulates T and B lymphocyte subsets and urinary CD80 excretion inpatients with steroid-dependent nephrotic syndrome. Pediatric Research, July 2018.

5. Ryter SW, BhatiaD and Choi ME. Autophagy: a Lysosome-Dependent Process with Implications in Cellular Redox Homeostasis and Human Disease. Antioxidants& Redox Signaling.Feb., 2018.

6. Khandelwal P*, BirlaS*, Bhatia D*, Puraswani M, Saini H., Sinha A., Hari P., SharmaA.,Bagga A. *Authors contributed equally. Mutations in membrane cofactor protein (CD46) gene in Indian children with hemolytic uremicsyndrome. Clin Kid Journal,August, 2017.

7. Sinha A, BhatiaD, Gulati A, Rawat M, Dinda AK, Hari P, Bagga A. Efficacy and safety ofrituximabin children with difficult-to-treat nephrotic syndrome. Nephrol. Dial.Transplant. Jan., 2015.

8. Bhatia D, KhandelwalP, Sinha A, Hari P, Cheong HI, Bagga A. Incomplete penetrance of CD46 mutation causing familial atypical hemolytic uremic syndrome. Pediatr Nephrol. Dec., 2015.

9. Sinha A, Gulati A,Saini S, Blanc C, Gupta A,Gurjar BS, Saini H, Kotresh ST, Ali U, Bhatia D et al.  Prompt plasma. exchanges and immunosuppressive treatment improves the outcomes of anti-factor H autoantibody-associated hemolytic uremic syndrome in children. Kidney Int., May, 2014.

10. Sinha A, Bajpai J, Saini S, Bhatia D, Gupta APuraswani M,Dinda AK, Agarwal SK, SaporyS, Pandey RM, Hari P, Bagga A. Serum soluble urokinase receptor levels do not distinguish focal segmental glomerulosclerosis from other causes of nephrotic syndrome in children. Kidney Int. March,2014.


11.  ChungKP, Hsu CL, Fan LC, HuangZ, Bhatia D,Chen YJ, Hisata S, Cho SJ, Nakahira K, Imamura M, ChoiME, Yu CJ, Cloonan SM,and Choi AMK. Mitofusins Regulate Lipid Metabolism toMediate the Development of Lung Fibrosis. Accepted by Nature Communications.

12. Bhatia D,Chung KP, Nakahira K, Patino E, Rice M, Torres L, Muthukumar T, Choi AMK, Akchurin O, Choi ME. Mitophagy Dependent Macrophage Reprogramming Protects against Kidney Fibrosis. Under consideration by the Journal of Clinical Investigation (submitted on June 24, 2019).