Ma Kunling, M.D., Ph.D.

Position: Chair of Nephrology

Department: Nephrology

Medical School: Zhejiang University School of Medicine, China

Academic Rank: Chief Physician



Appointment

Clinical / Research Interests

Diabetic Nephropathy;

Atherosclerosis;

Microinflammation and metabolic disorder of glucose and lipid-mediated target organ injuries  


Professional Highlights

Huaxia Medical Science and Technology Award, Third Prize

Jiangsu Medical Science and Technology Award, Second Prize

Jiangsu Science and Technology Progress Award, Second Prize

Nanjing Science and Technology Progress Award, Second Prize

Natural Science Award of Ministry of Education, First Prize

Zhejiang Science and Technology Progress Award, First Prize

Chinese Medical Science and Technology Award, Third Prize

Science and Technology Progress Award of Ministry of Education, Second Prize


Professional Appointments

Member, Renal Pharmacology Committee of the Chinese Pharmacological Society, 2021-present

Member, Renal Pathophysiology Committeeof the Chinese Society of Pathophysiology, 2019-2022

Member, Lipid and Lipoprotein Committee of the Chinese Society of Biochemistry, 2019-2022

Member, Nephrology Committee of Jiangsu Medical Association, 2019-2022

The 10th Youth Member of Kidney Disease of Chinese Medical Association, 2015-2018


Education Experience

Research Summary

GPR43 deficiency protects against podocyte insulin resistance in diabetic nephropathy through the restoration of AMPKα activity.

Dysbiosis of intestinal microbiota mediates tubulointerstitial injury in diabetic nephropathy via the disruption of cholesterol homeostasis.

Platelet microparticles mediate glomerular endothelial injury in early diabetic nephropathy.


Publications

Lu J, Chen PP, Zhang JX, Li XQ, Wang GH, Yuan BY, Huang SJ, Liu XQ, Jiang TT, Wang MY, Liu WT, Ruan XZ, Liu BC, Ma KL(*). GPR43 deficiency protects against podocyte insulin resistance in diabetic nephropathy through the restoration of AMPKα activity. Theranostics. 2021 Mar 4;11(10):4728-4742. (IF=11.556).

Lu CC, Hu ZB, Wang R, Hong ZH, Lu J, Chen PP, Zhang JX, Li XQ, Yuan BY, Huang SJ, Ruan XZ, Liu BC, Ma KL(*). Gut microbiota dysbiosis-induced activation of the intrarenal renin-angiotensin system is involved in kidney injuries in rat diabetic nephropathy. Acta Pharmacol Sin 2020 Aug;41(8):1111-1118. (IF=6.15).

Hu ZB, Lu J, Chen PP, Lu CC, Zhang JX, Li XQ, Yuan BY, Huang SJ, Ruan XZ, Liu BC, Ma KL(*). Dysbiosis of intestinal microbiota mediates tubulointerstitial injury in diabetic nephropathy via the disruption of cholesterol homeostasis. Theranostics 2020;10(6):2803-2816. (IF=11.556).

Lu J, Hu ZB, Chen PP, Lu CC, Zhang JX, Li XQ, Yuan BY, Huang SJ, *Ma KL. Urinary levels of podocyte-derived microparticles are associated with the progression of chronic kidney disease. Ann Transl Med. 2019 Sep;7(18):445. (IF=3.932).

Lu J, Hu ZB, Chen PP, Lu CC, Zhang JX, Li XQ, Yuan BY, Huang SJ, *Ma KL. Urinary podocyte microparticles are associated with disease activity and renal injury in systemic lupus erythematosus. BMC Nephrol. 2019 Aug 5;20(1):303.  (IF=2.388).

*Ma KL, Liu L, Zhang Y, Wang GH, Hu ZB, Chen PP, Lu J, Lu CC, Gong TK, Gong YX, Liu BC. Aspirin attenuates podocyte injury in diabetic rats through overriding cyclooxygenase-2-mediated dysregulation of LDL receptor pathway. Int Urol Nephrol. 2019 Mar;51(3):551-558. (IF=2.370)

Wang GH, *Ma KL, Zhang Y, Hu ZB, Liu L, Lu J, Chen PP, Lu CC, Ruan XZ, Liu BC. Caspase 3/ROCK1 pathway mediates high glucose-induced platelet microparticles shedding. Biochem Biophys Res Commun. 2019 Feb 5;509(2):596-602. (IF=3.575)

Wang GH, *Ma KL, Zhang Y, Hu ZB, Liu L, Lu J, Chen PP, Lu CC, Ruan XZ, Liu BC. Platelet microparticles contribute to aortic vascular endothelial injury in diabetes via the mTORC1 pathway. Acta Pharmacol Sin. 2019 Apr;40(4):468-476. (IF=6.15).

Wang GH, Lu J, *Ma KL, Zhang Y, Hu ZB, Chen PP, Lu CC, Zhang XL, Liu BC. The Release of Monocyte-Derived Tissue Factor-Positive Microparticles Contributes to a Hypercoagulable State in Idiopathic Membranous Nephropathy. J Atheroscler Thromb. 2019 Jun 1;26(6):538-546. (IF=4.928).

Zhang Y, *Ma KL, Gong YX, Wang GH, Hu ZB, Liu L, Lu J, Chen PP, Lu CC, Ruan XZ, Liu BC. Platelet Microparticles Mediate Glomerular Endothelial Injury in Early Diabetic Nephropathy. J Am Soc Nephrol. 2018;29(11):2671-2695.  (IF=10.121).

*Ma KL, Gong TK, Hu ZB, Zhang Y, Wang GH, Liu L, Chen PP, Lu J, Lu CC, Liu BC. Lipoprotein(a) accelerated the progression of atherosclerosis in patients with end-stage renal disease. BMC Nephrol. 2018;19(1):192. (IF=2.388).

*Ma KL, Wu Y, Zhang Y, Wang GH, Hu ZB, Ruan XZ. Activation of the CXCL16/CXCR6 pathway promotes lipid deposition in fatty livers of apolipoprotein E knockout mice and HepG2 cells. Am J Transl Res. 2018;10(6):1802-1816. (IF=4.060).

Lu CC, *Ma KL, Ruan XZ, Liu BC. Intestinal dysbiosis activates renal renin-angiotensin system contributing to incipient diabetic nephropathy. Int J Med Sci. 2018;15(8):816-822. (IF=3.738).

Hu ZB, *Ma KL, Zhang Y, Wang GH, Liu L, Lu J, Chen PP, Lu CC, Liu BC. Inflammation-activated CXCL16 pathway contributes to tubulointerstitial injury in mouse diabetic nephropathy. Acta Pharmacol Sin. 2018;39(6):1022-1033. (IF=6.15).

Lu CC, *Ma KL, Ruan XZ, Liu BC. The Emerging Roles of Microparticles in Diabetic Nephropathy. Int J Biol Sci. 2017 Sep 5;13(9):1118-1125. (IF=6.580).

#Hu ZB, #Chen Y, Gong YX, Gao M, Zhang Y, Wang GH, Tang RN, Liu H, Liu BC, *Ma KL. Activation of the CXCL16/CXCR6 Pathway by Inflammation Contributes to Atherosclerosis in Patients with End-stage Renal Disease. Int J Med Sci. 2016;13(11):858-867. (IF=3.738).

Wu Y, *Ma KL, Zhang Y, Wen Y, Wang GH, Hu ZB, Liu L, Lu J, Chen PP, Ruan XZ, Liu BC. Lipid disorder and intrahepatic renin-angiotensin system activation synergistically contributes to non-alcoholic fatty liver disease. Liver Int. 2016; 36(10):1525-34. (IF=5.828)

Zhang Y, *Ma KL, Ruan XZ, Liu BC. Dysregulation of the Low-Density Lipoprotein Receptor Pathway Is Involved in Lipid Disorder-Mediated Organ Injury. Int J Biol Sci. 2016; 12(5):569-79. (IF=6.580)

*Ma KL, Zhang Y, Liu J, Wu Y, Hu ZB, Liu L, Liu BC. Inflammatory stress induces lipid accumulation in multi-organs of db/db mice. Acta Biochim Biophys Sin (Shanghai). 2015; 47(10): 767-74. (IF=3.848).

Zhang Y, *Ma KL, Liu J, Wu Y, Hu ZB, Liu L, Liu BC. Dysregulation of low-density lipoprotein receptor contributes to podocyte injuries in diabetic nephropathy. Am J Physiol Endocrinol Metab. 2015; 308(12): E1140-8. (IF=4.310).

Zhang Y, *Ma KL, Liu J, Wu Y, Hu ZB, Liu L, Lu J, Zhang XL, Liu BC. Inflammatory stress exacerbates lipid accumulation and podocyte injuries in diabetic nephropathy. Acta Diabetol. 2015; 52(6):1045-56. (IF=4.280).

Liu J, *Ma KL, Zhang Y, Wu Y, Hu ZB, Lv LL, Tang RN, Liu H, Ruan XZ, Liu BC. Activation of mTORC1 disrupted LDL receptor pathway: a potential new mechanism for the progression of non-alcoholic fatty liver disease. Int J Biochem Cell Biol. 2015; 61: 8-19.  (IF=5.085)

*Ma KL, Zhang Y, Liu J, Wu Y, Hu ZB, Ruan XZ, Liu BC. Establishment of an Inflamed Animal Model of Diabetic Nephropathy. Int J Biol Sci 2014; 10(2): 149-159.  (IF=6.580)

Ma KL, Liu J, Gao M, Wang CX, Ni J, Zhang Y, Zhang XL, Liu H, Wang YL, *Liu BC. Activation of mTOR contributes to foam cell formation in the radial arteries of patients with end-stage renal disease. Clin Nephrol. 2014; 81(6):396-404.(IF=0.975)

Ma KL, Ni J, Wang CX, Liu J, Zhang Y, Wu Y, Lv LL, Ruan XZ, *Liu BC. Interaction of RAS Activation and Lipid Disorders Accelerates the Progression of Glomerulosclerosis. Int J Med Sci 2013; 10(12):1615-24. (IF=3.738)

Ma KL, Liu J, Wang CX, Ni J, Zhang Y, Wu Y, Lv LL, Ruan XZ, Liu BC. Activation of mTOR modulates SREBP-2 to induce foam cell formation through increased retinoblastoma protein phosphorylation. Cardiovasc Res 2013; 100(3):450-60. (IF=10.787).

Ni J, *Ma KL, Wang CX, Liu J, Zhang Y, Lv LL, Ni HF, Chen YX, Ruan XZ, Liu BC. Activation of renin-angiotensin system is involved in dyslipidemia-mediated renal injuries in apolipoprotein E knockout mice and HK-2 cells. Lipids Health Dis 2013; 12(1):49. (IF=3.876). 

Ma KL, Liu J, Ni J, Zhang Y, Lv LL, Tang RN, Ni HF, Ruan XZ, *Liu BC. Inflammatory stress exacerbates the progression of cardiac fibrosis in high-fat-fed apolipoprotein E knockout mice via endothelial-mesenchymal transition. Int J Med Sci 2013; 10(4):420-6. (IF=3.738). 

*Ma KL, Wang CX. Analysis of the spectrum and antibiotic resistance of uropathogens in vitro: results based on a retrospective study from a tertiary hospital. Am J Infect Control 2013; 41(7):601-6. (IF=2.918)

Liu J, *Ma KL, Gao M, Wang CX, Ni J, Zhang Y, Zhang XL, Liu H, Wang YL, Liu BC. Inflammation disrupts the LDL receptor pathway and accelerates the progression of vascular calcification in ESRD patients. PLoS One 2012; 7(10): e47217.  (IF=3.240). 

Ma KL, Varghese Z, Ku Y, Powis SH, Chen Y, Moorhead JF, *Ruan XZ. Sirolimus inhibits endogenous cholesterol synthesis induced by inflammatory stress in human vascular smooth muscle cells. Am J Physiol Heart Circ Physiol 2010; 298(6):H1646-51.  (IF=4.733).

Ma KL, *Ruan XZ, Powis SH, Chen YX, Moorhead JF, and Varghese Z. Inflammatory stress exacerbates lipid accumulation in hepatic cells and fatty livers of apolipoprotein E knockout mice. Hepatology 2008; 48 (3):770-81. (IF=17.425). 

Ma KL, *Ruan XZ, Powis SH, Chen Y, Moorhead JF, Varghese Z. Sirolimus modifies cholesterol homeostasis in hepatic cells: a potential molecular mechanism for sirolimus-associated dyslipidemia. Transplantation 2007; 84(8):1029-36.  (IF=4.939). 

Ma KL, *Ruan XZ, Powis SH, Moorhead JF, and Varghese Z. Anti-atherosclerotic effects of sirolimus on human vascular smooth muscle cells. Am J Physiol Heart Circ Physiol 2007; 292 (6):H2721-8. (IF=4.733). 


Current Program

The S-sulfhydrylation modification disorder of TST/VLCAD mediates tubulointerstitial injury in diabetic nephropathy, 2022-2025. Funding Source: National Natural Science Foundation of China.

Study on the mechanisms of ACSS2 modulating Sirt1 pathway to contribute to podocyte injury in diabetic nephropathy, 2020-2023. Funding Source: National Natural Science Foundation of China.


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