John Cijiang He, MD, PhD
- PROFESSOR | Medicine, Nephrology
- PROFESSOR | Pharmacological Sciences
Research Topics:Diabetes, HIV/AIDS, Kidney, Signal Transduction, Systems Biology
Dr. John Cijiang He got his MD from Shanghai Second medical University in China and PhD in Physiology at University of Paris VII in France. Then, he got his further research training as a visiting scientist at NIH in Maryland and The Picower Institute for Medical Research in New York. He completed his medical residency at SUNY down state and clinical nephrology fellowship at Mount Sinai Hospital in New York. Currently, he is a Professor of Medicine and Pharmacological Sciences at Icahn School of Medicine at Mount Sinai. He holds the title of Irene and Dr. Arthur Fishberg endowed chair of Nephrology. He is the chief of Nephrology at Mount Sinai Health System. He was the President of the New York Society of Nephrology and the President of Chinese American Society of Nephrology. He is the member of the American Society of Clinical Investigation. He is also a visiting professor at both Nanjing University and Shanghai Jiaotong University. He has been funded by multiple NIH and VA grants and has published more than 180 papers in the peer-reviewed scientific journals. His major research areas include glomerular cell biology, systems biology of kidney disease, and kidney fibrosis. His major clinical interest includes diabetic kidney disease, viral-induced kidney disease, and primary glomerular disease.
American Board of Internal Medicine
- Diabetic Kidney Disease
- Kidney Failure
Multi-Disciplinary Training AreaBiophysics and Systems Pharmacology [BSP]
MD, Shanghai 2nd Medical School
MD, Shanghai Second Medical College
MS, University of Paris VII
Rui-Jin Hospital, Shanghai 2nd Medical School
PhD, University of Paris VII
SUNY Health Science Center
SUNY Health Science Center
The Mount Sinai Medical Center
Residency, Internal Medicine, S.U.N.Y., Health Science Center
Fellowship, Metabolic Diseases, National Institutes of Health
Fellowship, Renal Medicine, Mount Sinai Hospital
Role of HIPK2 in kidney fibrosis
We have identified that HIPK2 plays a key role in kidney fibrosis. We are studying the mechanism of HIPK2 in mediating kidney fibrosis and try to identify potential anti-fibrosis therapy by targeting HIPK2. Please visit the He Laboratory.
Pathogenesis of diabetic kidney disease
We are studying the role of advanced glycation endproducts (AGE) and oxidative stress in podocyte injury and diabetic kidney disease. We are studying the role and the post-translational regulation (acetylation) of key transcription factors such as FOXO, NF-kB and Stat3 in mediating podocyte injury and diabetic kidney disease.
Podocyte Biology and Pathology
We are studying the signaling network that mediates podocyte differentiation and injury using both in vitro and in vivo models. We are studying the relationship between mechanical force, morphology, and chemical signals and their role in maintaining normal podocyte differentiation status. We are studying the mechanism of podocyte injury in diabetic kidney disease and HIV-associated nephropathy. We are studying how retinoic acid could repair podocyte injury through induction of differentiation and regeneration process.
Using systems biology approach to study kidney disease
We are using systems biology approach to study cell signaling and gene transcription networks in kidney disease. We are studying the transcriptome, epigenome and proteome in injured podocytes and diseased kidney. We are using systems pharmacology approach to identify new drug targets or therapy for kidney disease.
Pathogenesis of HIV-Associated Nephropathy
We are studying the role of HIV viral protein in the development of HIV-associated nephropathy. The role and signaling pathways of HIV Nef have been studied in kidney podocytes. We are also investigating the mechanism of chronic HIV infection on the progression of other kidney diseases such as diabetic nephropathy and hypertensive kidney disease.
- Effects of Glycoxidative Stress on Human Aging
The purpose of this study is to explore the efficacy of Low AGE Diet, a new intervention, based on reduced oral intake of glycotoxins (AGEs), on inflammation and major chronic diseases of aging, such as diabetes, vascular, kidney and Alzheimer's diseases.
Retinoic acid improves nephrotoxic serum-induced glomerulonephritis through activation of retinoic acid receptor alpha. Kidney Int 2017 july;.
A novel HIPK2 inhibitor mitigates kidney fibrosis through inhibition of TGF-Smad3 pathway. J Am Soc, Nephrol. 2017 Jul; 28(7): 2133-2143.
Inhibition of rtn1a-mediated ER stress at early stage of kidney injury attenuates progression of renal fibrosis. J Am Soc Nephrol 2017 Jul; 28(7): 2007-2021.
Krüppel-like factor 15 mediates glucocorticoid-induced restoration of podocyte differentiation markers. J. Am Soc Nephrol 2016 Jun;.
Comparison of Glomerular and Podocyte mRNA Profiles in eNOS-/- Diabetic Mice Induced by Streptozotocin. J. Am. Soc. Nephrol 2016 Apr; 27(4): 1006-14.
RTN1 is a novel mediator for progression of kidney disease. Nat Commun 2015 Jul; 31(6): 7841.
Krüppel-like factor 6 regulates mitochondrial function in the kidney. J Clin. Invest 2015 Marc;: 1347-61.
An intronic locus determines SHROOM3-expression and potentiates renal allograft fibrosis. J. Clin. Invest. 2015 Jan; 2(125): 208-21.
Nephrin preserves podocyte viability and glomerular structure and function in adult mice. Am. J Soc. Nephrol 2015 Feb;.
Induction of retinol dehydrogenase 9 expression in podocytes attenuates kidney injury. J. Am Soc Nephrol 2014 Sept; 25(9): 1933-41.
Dai Y, Gu L, Yuan W, Yu Q, Ni Z, Ross M, Kaufman L, Xiong H, Salant D, He J, Chuang P. Podocyte-Specific Deletion of Signal Transducer and Activator of Transcription 3 Attenuates Nephrotoxic Serum-Induced Glomerulonephritis. Kidney Int 2013 Nov; 84(5): 950-61.
Mallipattu SK, Liu R, Zhong Y, Chen EY, D'Agati V, Kaufman L, Ma'ayan A, Klotman PE, Chuang PY, He JC. Renal-protective effect for ACEI and HDACI inferred from CMAP. J. Am. Soc. Nephrol 2013 Apr; 24(5): 801-11.
Jiang S, Chuang P, Liu Z, He J. Outcomes of systems biology approaches in primary glomerular diseases. Nat. Rev. Nephrol. 2013 Sep; 9(9): 500-12.
Jin Y, Ratnam K, Chuang PY, Fan Y, Zhong Y, Dai Y, Mazloom AR, Chen EY, D'Agati V, Xiong H, Ross MJ, Chen N, Ma'ayan A, He JC. Systems approach identifies HIPK2 as a key regulator of kidney fibrosis. Nature medicine 2012 Apr; 18(4).
Role of Retinoic Acid Receptor-alpha in HIV-associated Nephropathy. Kidney Int 2011 Mar; 79(6): 624-34.
Feng X, Lu T, Chuang P, Fang W, Krishna R, Xiong H, Ouyang X, Shen Y, Levy D, Hyink D, Klotman M, D'Agati V, Iyengar R, Kotman P, He J. Knock-down of Stat3 activity in vivo attenuates HIV-induced kidney injury. J. Am Soc Nephrol 2009 Oct; 20: 2138-46.
Lu C, He C, Cai W, Liu H, Zhu L, Vlassara H. AGE-receptor-1 is a negative regulator of the RAGE-promoted inflammatory response to advanced glycation endproducts in mesangial cells. Proc. Natl. Acad. Sci. U.S.A; 101: 11767-11772.
Hardy SV, Eungdamrong NJ, Chen Y, Jayaraman G, Chuang PY, Fang W, Xiong H, Neves SR, Jain MR, Li H, Ma'ayan A, Gordon RE, He JC, Iyengar R. Nef stimulates proliferation of glomerular podocytes through activation of Src-dependent Stat3 and MAPK1,2 pathways. J. Clin. Invest; 114: 643-651.
Reactive Advanced Glycation Endproducts from food: a new risk for diabetic complications. Proc. Natl. Acad. Sci. U.S.A., 1997; 94: 6474-6479.
He C, Esposito C, Phillips C, Zalups RK, Henderson DA, Striker GE, Striker LJ. Dissociation of glomerular hypertrophy, cell proliferation, and glomerulosclerosis in mouse strains heterozygous for a mutation (Os) which induces a 50% reduction in nephron number. The Journal of clinical investigation 1996 Mar; 97(5).