Jianjie Ma

Jianjie Ma
Occupation(s)Researcher, entrepreneur, and academic
Academic background
EducationB.S., Physics
Ph.D., Physiology and Biophysics
Alma materWuhan University
Baylor College of Medicine
Academic work
InstitutionsUniversity of Virginia

Jianjie Ma is researcher, entrepreneur and academic. He is the William H. Muller Professor and director of Surgical Sciences at the University of Virginia.[1]

Ma's research encompasses muscle physiology, cardiovascular disease, regenerative medicine, immune modulation, cancer therapy, geriatric medicine, diabetes, and Alzheimer’s disease. In collaboration with Hiroshi Takeshima of, he has identified MG53, a muscle-specific tripartite motif protein essential for cell membrane repair as well as the TRiC family of counter-ion channels critical for excitation-contraction (E-C) coupling in muscle cells.

As of 2025, Ma's work has been cited 19,700 times according to Scopus.[2]

Education

Ma completed his B.S degree in Physics from Wuhan University in 1983. In 1989, he earned a Ph.D. in Physiology and Biophysics from Baylor College of Medicine and completed his postdoctoral studies from Rush University School of Medicine in 1991.[3]

Career

Ma began his academic career as assistant professor at the Rush University (1991 – 1992), followed by an appointment at Case Western Reserve University (CWRU) (1992 – 1996). In 1996, he was promoted to associate professor at CWRU and remained at the post until 2001. In 2001, he joined Robert Wood Johnson Medical School (RWJMS) at Rutgers University as a university-named professor and remained there until 2012. Between 2012 and 2022, he held the Karl P. Klassen Chair in Thoracic Surgery at Ohio State University (OSU), where he was also the vice chair of research in the Department of Surgery. In 2022, he joined the University of Virginia as the William H. Muller Endowed Professor.[3]

Since 2022, Ma has been the director of the Division of Surgical Sciences at the University of Virginia. He has founded three biotechnology companies: TRIM-edicine, MGMedicine, and HTIC.[3]

Research

Ma has used different animal models, molecular and cellular imaging, gene editing, and delivery tools to investigate the physiologic function of novel genes in health and disease. Ma's early research has contributed to the identification of the ryanodine receptor as a functional calcium release channel and identified store-operated calcium entry (SOCE) in skeletal muscle excitable cells.[4] His research also uncovered the function of SOCE in excitable muscle cells, highlighting its critical role in muscle function during exercise, fatigue, ageing, and muscular dystrophy.[5][6]

Ma investigated the structure–function relationship of the cystic fibrosis transmembrane conductance regulator (CFTR) as a chloride channel. He identified a critical region within the regulatory (R) domain that modulates channel activity,[7] and demonstrated that certain CFTR processing mutants retain functional chloride channel activity when reconstituted into lipid bilayer membranes.[8]

Alongside colleagues, Ma also explored mechanisms of mitochondrial apoptosis, highlighting that calcium flux and pro-apoptotic proteins contribute to mitochondrial-mediated cell death.[9]

In collaboration with Hiroshi Takeshima, Ma's research focused on defining the molecular framework of E-C coupling and its relevance to human disease and regenerative medicine. The collaboration resulted in the description of TRIC channels as essential for intracellular calcium handling.[10] Their work also identified MG29, a synaptophysin-family protein involved in transverse-tubule biogenesis and calcium signaling.[11] This collaboration also resulted in the discovery of MG53, a key component of the cell membrane repair machinery.[12] Subsequent studies demonstrated that MG53 possesses potent anti-inflammatory and tissue-protective properties across a range of disease models.[13]

Ma’s research on Alzheimer's disease focused on the neuroprotective and anti-inflammatory properties of MG53,[14] and were undertaken to develop strategies for the prevention of cognitive decline associated with neuroinflammation.[15] He has also contributed to the development of an exercise pill aimed at treating diabetes.[16]

As of 2025, Ma's work has been cited 19,700 times according to Scopus.[2]

Awards and honors

Selected articles

  • Smith, J S; Imagawa, T; Ma, J; Fill, M; Campbell, K P; Coronado, R (July 1, 1988). "Purified ryanodine receptor from rabbit skeletal muscle is the calcium-release channel of sarcoplasmic reticulum". Journal of General Physiology. 92 (1): 1–26. doi:10.1085/jgp.92.1.1. ISSN 0022-1295. PMC 2228891. PMID 2459298.
  • Ma, Jianjie; Fill, Michael; Knudson, C. Michael; Campbell, Kevin P.; Coronado, Roberto (October 7, 1988). "Ryanodine Receptor of Skeletal Muscle Is a Gap Junction-Type Channel". Science. 242 (4875): 99–102. Bibcode:1988Sci...242...99M. doi:10.1126/science.2459777. PMID 2459777.
  • Cai, Chuanxi; Masumiya, Haruko; Weisleder, Noah; Matsuda, Noriyuki; Nishi, Miyuki; Hwang, Moonsun; Ko, Jae-Kyun; Lin, Peihui; Thornton, Angela; Zhao, Xiaoli; Pan, Zui; Komazaki, Shinji; Brotto, Marco; Takeshima, Hiroshi; Ma, Jianjie (February 1, 2009). "MG53 Nucleates Assembly Of Cell Membrane Repair Machinery". Biophysical Journal. 96 (3): 361a. Bibcode:2009BpJ....96..361C. doi:10.1016/j.bpj.2008.12.1824. ISSN 0006-3495.
  • Calcraft, Peter J.; Ruas, Margarida; Pan, Zui; Cheng, Xiaotong; Arredouani, Abdelilah; Hao, Xuemei; Tang, Jisen; Rietdorf, Katja; Teboul, Lydia; Chuang, Kai-Ting; Lin, Peihui; Xiao, Rui; Wang, Chunbo; Zhu, Yingmin; Lin, Yakang; Wyatt, Christopher N.; Parrington, John; Ma, Jianjie; Evans, A. Mark; Galione, Antony; Zhu, Michael X. (May 2009). "NAADP mobilizes calcium from acidic organelles through two-pore channels". Nature. 459 (7246): 596–600. Bibcode:2009Natur.459..596C. doi:10.1038/nature08030. ISSN 1476-4687. PMC 2761823. PMID 19387438.
  • Cheng, Chunming; Ru, Peng; Geng, Feng; Liu, Junfeng; Yoo, Ji Young; Wu, Xiaoning; Cheng, Xiang; Euthine, Vanessa; Hu, Peng; Guo, Jeffrey Yunhua; Lefai, Etienne; Kaur, Balveen; Nohturfft, Axel; Ma, Jianjie; Chakravarti, Arnab; Guo, Deliang (November 9, 2015). "Glucose-Mediated N-glycosylation of SCAP Is Essential for SREBP-1 Activation and Tumor Growth". Cancer Cell. 28 (5): 569–581. doi:10.1016/j.ccell.2015.09.021. ISSN 1535-6108. PMC 4643405. PMID 26555173.

References

  1. ^ Rivera, Luis Soler (2024-06-03). "Researcher Highlight Q&A: Jianjie Ma, PhD, Gene Function & Cardiovascular Disease". Healthy Practice. Retrieved 2025-06-22.
  2. ^ a b "Jianjie Ma". Scopus. Retrieved 17 June 2025.
  3. ^ a b c d "Jianjie Ma" (PDF). Jianjie Ma Lab. Retrieved May 28, 2025.
  4. ^ Bezprozvanny, I; Ehrlich, B E (1 November 1994). "Inositol (1,4,5)-trisphosphate (InsP3)-gated Ca channels from cerebellum: conduction properties for divalent cations and regulation by intraluminal calcium". The Journal of General Physiology. 104 (5): 821–856. doi:10.1085/jgp.104.5.821. PMC 2229238. PMID 7876825.
  5. ^ Frontera, Walter R.; Ochala, Julien (March 2015). "Skeletal Muscle: A Brief Review of Structure and Function". Calcified Tissue International. 96 (3): 183–195. doi:10.1007/s00223-014-9915-y. PMID 25294644.
  6. ^ Cheng, Heping; Lederer, W. J. (October 2008). "Calcium Sparks". Physiological Reviews. 88 (4): 1491–1545. doi:10.1152/physrev.00030.2007. PMID 18923188.
  7. ^ Hwang, Tzyh-Chang; Yeh, Jiunn-Tyng; Zhang, Jingyao; Yu, Ying-Chun; Yeh, Han-I; Destefano, Samantha (2 April 2018). "Structural mechanisms of CFTR function and dysfunction". Journal of General Physiology. 150 (4): 539–570. doi:10.1085/jgp.201711946. PMC 5881446. PMID 29581173.
  8. ^ Hume, Joseph R.; Duan, Dayue; Collier, Mei Lin; Yamazaki, Jun; Horowitz, Burton (1 January 2000). "Anion Transport in Heart". Physiological Reviews. 80 (1): 31–81. doi:10.1152/physrev.2000.80.1.31. PMID 10617765.
  9. ^ Wen, Shijun; Zhu, Daqian; Huang, Peng (January 2013). "Targeting Cancer Cell Mitochondria as a Therapeutic Approach". Future Medicinal Chemistry. 5 (1): 53–67. doi:10.4155/fmc.12.190. PMC 3587793. PMID 23256813.
  10. ^ Padhy, Biswajit; Xie, Jian; Wang, Runping; Lin, Fang; Huang, Chou-Long (August 2022). "Channel Function of Polycystin-2 in the Endoplasmic Reticulum Protects against Autosomal Dominant Polycystic Kidney Disease". Journal of the American Society of Nephrology. 33 (8): 1501–1516. doi:10.1681/ASN.2022010053. PMC 9342640. PMID 35835458.
  11. ^ Carrasco, Silvia; Meyer, Tobias (7 July 2011). "STIM Proteins and the Endoplasmic Reticulum-Plasma Membrane Junctions". Annual Review of Biochemistry. 80 (1): 973–1000. doi:10.1146/annurev-biochem-061609-165311. PMC 3897197. PMID 21548779.
  12. ^ Blazek, Alisa D.; Paleo, Brian J.; Weisleder, Noah (November 2015). "Plasma Membrane Repair: A Central Process for Maintaining Cellular Homeostasis". Physiology. 30 (6): 438–448. doi:10.1152/physiol.00019.2015. PMC 4630197. PMID 26525343.
  13. ^ Cooper, Sandra T.; McNeil, Paul L. (October 2015). "Membrane Repair: Mechanisms and Pathophysiology". Physiological Reviews. 95 (4): 1205–1240. doi:10.1152/physrev.00037.2014. PMID 26336031.
  14. ^ Paudel, Yam Nath; Angelopoulou, Efthalia; Piperi, Christina; Othman, Iekhsan; Aamir, Khurram; Shaikh, Mohd. Farooq (7 February 2020). "Impact of HMGB1, RAGE, and TLR4 in Alzheimer's Disease (AD): From Risk Factors to Therapeutic Targeting". Cells. 9 (2): 383. doi:10.3390/cells9020383. PMC 7072620. PMID 32046119.
  15. ^ "Mitigating neuroinflammation and enhancing neuronal integrity in Alzheimer's disease". NIH. Retrieved May 5, 2025.
  16. ^ Belcher, Craig (April 28, 2023). "Betting on biotech". Virginia Business.
  17. ^ "Jianjie Ma, PhD and Megan Tracci, MD Honored with 2025 Dean's Awards". University of Virginia. 28 January 2025. Retrieved April 28, 2025.
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