Photo of John Ci-jiang He

John Ci-jiang He

  • PROFESSOR Medicine, Nephrology
  • PROFESSOR Pharmacology and Systems Therapeutics
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Education

  • M.D., Shanghai 2nd Medical School

  • Rui-Jin Hospital, Shanghai 2nd Medical School
    General Medicine

  • M.S., University of Paris VII
    Physiology

  • Tenon Hospital
    Nephrology

  • Ph.D., University of Paris VII

  • Tenon Hospital
    INSERM U 64

  • SUNY Health Science Center
    General Medicine

  • SUNY Health Science Center
    General Medicine

  • The Mount Sinai Medical Center
    Nephrology

Biography

    Dr. John Cijiang He is a former graduate from Shanghai Second medical University. He got his PhD in Physiology at University of Paris VII, 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 tenured full Professor of Medicine and Pharmacology/Systems Therapeutics 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 division chief of Nephrology at both Mount Sinai Hospital and James J Peters Veteran Affair medical Center. He was the past President of the New York Society of Nephrology. Currently, he is the President of Chinese American Society of Nephrology. 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 100 papers in the peer-reviewed scientific journals. His major research areas include podocyte biology and pathology, signaling networks in kidney cells, systems biology of kidney disease, and kidney fibrosis. His major clinical interest includes diabetic kidney disease, viral-induced kidney disease, and primary glomerular disease.

Research

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.

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.

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.

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.

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.

Publications

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).

He JC, Husain M, Sunamoto M, D'Agati VD, Klotman ME, Iyengar R, Klotman PE. Nef stimulates proliferation of glomerular podocytes through activation of Src-dependent Stat3 and MAPK1,2 pathways. The Journal of clinical investigation 2004 Sep; 114(5).

Cai W, He JC, Zhu L, Lu C, Vlassara H. Advanced glycation end product (AGE) receptor 1 suppresses cell oxidant stress and activation signaling via EGF receptor. Proceedings of the National Academy of Sciences of the United States of America 2006 Sep; 103(37).

Chuang PY, Yu Q, Fang W, Uribarri J, He JC. Advanced glycation endproducts induce podocyte apoptosis by activation of the FOXO4 transcription factor. Kidney international 2007 Oct; 72(8).

Korgaonkar SN, Feng X, Ross MD, Lu TC, D'Agati V, Iyengar R, Klotman PE, He JC. HIV-1 upregulates VEGF in podocytes. Journal of the American Society of Nephrology : JASN 2008 May; 19(5).

Lu TC, Wang Z, Feng X, Chuang P, Fang W, Chen Y, Neves S, Maayan A, Xiong H, Liu Y, Iyengar R, Klotman PE, He JC. Retinoic acid utilizes CREB and USF1 in a transcriptional feed-forward loop in order to stimulate MKP1 expression in human immunodeficiency virus-infected podocytes. Molecular and cellular biology 2008 Sep; 28(18).

Feng X, Lu TC, Chuang PY, Fang W, Ratnam K, Xiong H, Ouyang X, Shen Y, Levy DE, Hyink D, Klotman M, D'Agati V, Iyengar R, Klotman PE, He JC. Reduction of Stat3 activity attenuates HIV-induced kidney injury. Journal of the American Society of Nephrology : JASN 2009 Oct; 20(10).

Ratnam KK, Feng X, Chuang PY, Verma V, Lu TC, Wang J, Jin Y, Farias EF, Napoli JL, Chen N, Kaufman L, Takano T, D'Agati VD, Klotman PE, He JC. Role of the retinoic acid receptor-α in HIV-associated nephropathy. Kidney international 2011 Mar; 79(6).

Zhong Y, Wu Y, Liu R, Deng Y, Mallipattu SK, Klotman PE, Chuang PY, He JC. Roflumilast enhances the renal protective effects of retinoids in an HIV-1 transgenic mouse model of rapidly progressive renal failure. Kidney international 2012 May; 81(9).

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. A systems approach identifies HIPK2 as a key regulator of kidney fibrosis. Nature medicine 2012 Apr; 18(4).

Mallipattu SK, Liu R, Zheng F, Narla G, Ma'ayan A, Dikman S, Jain MK, Saleem M, D'Agati V, Klotman P, Chuang PY, He JC. Kruppel-like factor 15 (KLF15) is a key regulator of podocyte differentiation. The Journal of biological chemistry 2012 Jun; 287(23).

Zhang G, Liu R, Zhong Y, Plotnikov AN, Zhang W, Zeng L, Rusinova E, Gerona-Nevarro G, Moshkina N, Joshua J, Chuang PY, Ohlmeyer M, He JC, Zhou MM. Down-regulation of NF-κB transcriptional activity in HIV-associated kidney disease by BRD4 inhibition. The Journal of biological chemistry 2012 Aug; 287(34).

Mallipattu SK, Liu R, Zhong Y, Chen EY, D'Agati V, Kaufman L, Ma'ayan A, Klotman PE, Chuang PY, He JC. Expression of HIV transgene aggravates kidney injury in diabetic mice. Kidney international 2013 Apr; 83(4).

Zhong Y, Chen EY, Liu R, Chuang PY, Mallipattu SK, Tan CM, Clark NR, Deng Y, Klotman PE, Ma'ayan A, He JC. Renoprotective effect of combined inhibition of angiotensin-converting enzyme and histone deacetylase. Journal of the American Society of Nephrology : JASN 2013 Apr; 24(5).

Azeloglu EU, 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. Interconnected network motifs control podocyte morphology and kidney function. Science Signal 2014 February; 7(311).

Industry Relationships

Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.

Below are financial relationships with industry reported by Dr. He during 2012 and/or 2013. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.

Other Activities: Examples include, but are not limited to, committee participation, data safety monitoring board (DSMB) membership.

  • Merck & Co., Inc.

Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.

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Fax: 212-987-0389