Qinglin Yang, Ph.D.

Professor, Cardiovascular Center of Excellence
Professor, Department of Pharmacology


(currently accepting Graduate Students and Post-doctoral Fellows)


Bachelor of Medicine, 1984
Guang Zhou University of Chinese Medicine, China

Master of Medicine, Pediatrics 1989
Guang Zhou University of Chinese Medicine, China

MS, Pharmacy, 1992
University of Montana, Missoula, MT

PhD, Cardiovascular Physiology, 1996
Washington State University, Pullman, WA


Dr. Qinglin Yang is a Professor in the Cardiovascular Center of Excellence and the Department of Pharmacology. Dr. Yang received his B.M. degree from Guang Zhou University of Chinese Medicine in Guang Zhou, China in 1984. He also received his M. M. degree from Guang Zhou University of Chinese Medicine in 1989. Dr. Yang moved to Montana where he received his M.S. degree in 1992 from the University of Montana in Missoula. Dr. Yang received his Ph.D. from Washington State University in 1996 under the mentorship of Dr. Bryan Slinker. His postdoctoral studies were completed in Dr. Jeffrey Robbins' lab at Cincinnati Children's Hospital Medical Center in 2000. Dr. Yang started his independent lab in the Cardiovascular Research Institute at Morehouse School of Medicine from 2000 and moved his lab to the Department of Nutrition at the University of Alabama at Birmingham in 2008. Dr. Yang and his research team joined the Cardiovascular Center of Excellence and Department of Pharmacology & Experimental Therapeutics at LSUHSC-New Orleans in August 2018. 

Research Interests

Research in our lab seeks to understand the molecular and biochemical mechanisms that drive the pathological growth, remodeling, and cell death of the heart. A normal adult heart functions almost exclusively aerobically, as evidenced by the high density of mitochondria in heart cells (cardiomyocytes). The transcriptional and biochemical regulation of mitochondrial energy metabolism plays a pivotal role in the heart to meet the high energy demand. However, it remains elusive as of how the transcriptional and biochemical regulation may alter to adapt to the pathological stresses in patients under conditions such as hypertension, infarct, and diabetes. Cardiomyocytes stop replicating shortly after birth, which coincides with the kick off of the aerobic metabolism of the heart for energy provision. Therefore, the proliferation and differentiation of cardiomyocytes appear to relate to a differential metabolic programs in the heart at different stages of development and pathophysiology.

Our team determines how altered metabolic programming is involved in the pathological development of the heart by dissecting potential pathways in cultured cells and genetically engineered mice that are subjected to various disease conditions. We seek to gain mechanistic insights at the cell, organelle, organ, and intact animal level using techniques in physiology, histology, cell biology and biochemistry integrated with various omics analyses. We also apply insights from the heart to other tissues and look further into the systemic and inter-tissue cross-talks at other disease states. The long-term goal is to understand the complex interactions that modulate genetic and metabolic reprogramming in the diseased heart, and to apply this information to novel clinical diagnostics and therapeutic strategies.

Research projects: 

1) Targeting the mitochondria to protect the ischemic diabetic heart (supported by American Diabetes Association)

2) Improving mitochondrial function to protect against myocardial ischemia/reperfusion (supported by NHLBI)

3) Restore energy capacity in the aging heart (supported by NIA)

Selected Publications

Selected publications:

Q. Yang, A. Sanbe, H. E. Osinska, R. Klevisky, T. E. Hewett, and J. Robbins: A mouse model of myosin binding protein C human familial hypertrophic cardiomyopathy. J. of Clinical Investigation 102, 1292-1300, 1998.

Q. Yang, A. Sanbe, H. E. Osinska, R. Klevisky, T. E. Hewett and J. Robbins: In vivo modeling of myosin binding protein C familial hypertrophic cardiomyopathy. Circulation Research 85 (9): 841-847, 1999. (On the cover).

Q. Yang, T. E. Hewett, R. Klevisky, A. Sanbe, Xuejun Wang and J. Robbins: PKA dependent phosphorylation of Cardiac Myosin binding Protein C in transgenic mice. Cardiovascular Research 51(1):80-8, 2001.

Q. Yang, Osinska H, R. Klevisky and J. Robbins: Phenotypic deficits in mice expressing a Myosin Binding Protein C lacking the Titin and Myosin binding domains. Journal of Molecular and Cellular Cardiology. 2001 Sep;33(9):1649-58

Cheng LH, Ding GL, Qin QH, Xiao Y, Woods D, Chen YE, Yang Q*. Peroxisome proliferator-activated receptor delta activates fatty acid oxidation in cultured neonatal and adult cardiomyocytes. Biochem Biophys Res Commun. 2004; 313(2):277-86. 

Cheng LH, Ding LH, Qin QH, Huang Y, Lewis W, He N, Evans RM, Schneider MD, Brako LA, Woods D, Xiao Y, Chen EY, and Yang Q*. Cardiomyocyte-restricted Peroxisome proliferator-activated receptor d deletion perturbs myocardial fatty acid fatty acid oxidation and leads to cardiomyopathy. Nature Medicine 2004; 10, 1245 – 1250.

Yang Q*, Cheng LH: Molecular regulation of lipotoxicity in the heart (Invited review) Drug Discovery Today: Disease mechanisms. 2005; 2(1), 101-107.

Ding G, Cheng LH, Qin QH, Frontin SE, Yang Q*: Peroxisome proliferator-activated receptor d inhibits cardiac TNFa expression in response to inflammatory stimuli. Journal of Molecular and Cellular Cardiology. 2006; 40(6):821-8. (On the cover).

Lee J, Hu Q, Nakamura Y, Wang X, Zhang X, Zhu X, Chen W, Yang Q*, Zhang J: Open-chest 31P Magnetic Resonance Spectroscopy of Mouse Heart at 4.7 Tesla. Journal of Magnetic Resonance Imaging.  2006 Dec;24(6):1269-76.

Yang Q* and YH Li: Roles of PPARs on regulating myocardial lipid homeostasis (Invited review). Journal of Molecular Medicine 2007:85(7):697-706.

Ding GL, Qin QH, Qin QH, He N, Cheng LH, Francis-David SC, Hou J, Ernest Ricks, Liu J and Yang Q*. Adiponectin and its receptors are expressed in cardiomyocytes and regulated by PPARg. Journal of Molecular and Cellular Cardiology. 2007 Jul;43(1):73-84. PMC1950729

Ding G, Fu M, Qin QH, Lewis W, Kim HW, Fukai T, Bacanamwo M, Chen EY, Schneider MD, Mangelsdorf DJ, Evans RM and Yang Q*: Peroxisome Proliferator-Activated Receptor g is essential in maintaining myocardial redox homeostasis. Cardiovascular Research. 2007, 76(2):269-79

Li YQ, Yin R, Liu J, Wang PY, Wu SJ, Luo JW, Zhelyabovska O, Yang Q*: Peroxisome Proliferator-activated Receptor d Regulates Mitofusin 2 Expression in the Heart. Journal of Molecular and Cellular Cardiology 2009:46(6):876-82. PMC2845388

Wu SJ, Yin R, Ernest R, Li YQ, Zhelyabovska O, Luo JW, Yang YF, Yang Q*: LXRα is a negative regulator of cardiac hypertrophy via suppressing NF-κB signaling. Cardiovascular Research. 2009 Oct 1;84(1):119-26. PMC2741346

Li Y, Cheng LH, Qin QH, Liu J, Lo WK, Brako LA and Yang Q*: High-fat feeding in cardiomyocyte-restricted PPARd knockout mice leads to cardiac overexpression of lipid metabolic genes but fails to recue cardiac phenotypes. Journal of Molecular and Cellular Cardiology 2009:47(4):536-43. PMC2766590

Wang P, Liu J, Li Y, Wu S, Luo J, Yang H, Subbiah R, Chatham J, Zhelyabovska O, Yang Q*: PPARd is an essential transcriptional regulator for mitochondrial protection and biogenesis in adult heart. Circulation Research. 2010 Mar 19;106(5):911-9. PMC2993321

Luo N, Tian L, Liu J, Chung BH, Yang Q, Klein RL, Garvey WT, Fu Y: Macrophage adiponectin expression improves body metabolism in vivo. Diabetes. 2010 Apr;59 (4):791-9. PMC2844826

Liu J, Wang P, Luo J, Huan Y, He L, Yang H, Li Q, Wu S, Zhelyabovska O and Yang Q*. PPARβ/δ activation in adult hearts facilitates mitochondrial function and protects cardiac performance under pressure-overload condition. Hypertension. 2011 Feb;57(2):223-30. NIHMSID # 265863

Liu J, Wang P, He L, Li Y, Luo J, Cheng L, Qin Q, Brako LA, Lo WK, Lewis W and Yang Q*. Cardiomyocyte-restricted deletion of PPARβ/δ in PPARα-null mice causes impaired mitochondrial biogenesis and defense, but no further depression of myocardial fatty acid oxidation. PPAR Research. 2011; 2011:372854. PMC3167180

He L, Kim TY, Long QQ, Liu J, Wang P, Ding YS, Zhou YQ, Prasain J, Wood PA, and Yang Q*: Carnitine palmitoyltransferase 1b (CPT1b) deficiency aggravates pressure-overload-induced cardiac hypertrophy due to lipotoxicity. Circulation. 2012 Oct 2;126(14):1705-16. (This paper has been listed as Circulation Editors’ Picks as one of the most read articles in heart failure).

Kim T, Zhelyakovska O, Liu J and Yang Q*: Generation of inducible, tissue-specific TG mouse lines with PPARd overexpression. Methods Mol Biol. 2013;952:57-65.

Kim T and Yang Q*: PPARs regulate redox signaling in the cardiovascular system. World Journal of Cardiology. 2013 Jun 26;5(6):164-74.

Ding Y, Yang KD and Yang Q*: The role of PPARd Signaling in the Cardiovascular System. Prog Mol Biol Transl Sci. 2014;121:451-73

Kim TY, He L, Johnson MS, Li Y, Zeng L, Ding Y, Long Q, Moore JF, Sharer JD, Nagy TR, Young ME, Wood PA and Yang Q*: Carnitine palmitoyltransferase 1b deficiency protects mice from diet-induced insulin resistance. J Diabetes Metab. 2014 2014 Apr 1;5(4):361. PMC4190034.

Kim TY, Moore JF, Sharer JD, Yang K, Philip A. Wood, Yang Q*: Carnitine palmitoyltransferase 1b deficient mice develop severe insulin resistance after prolonged high fat diet feeding. J Diabetes Metab. 2014;5. pii: 1000401. PMC4286342.

Long Q, Yang K, Yang Q*: Regulation of mitochondrial ATP synthase in cardiac pathophysiology. Am J Cardiovasc Dis 2015;5(1):19-32.

Magadum A, Ding Y, He L, Kim T, Dalvoy M, Renikunta HV, Weidinger G, Yang Q* and Engel FB*: Live cell screening platform identifies PPARδ as a regulator of cardiomyocyte proliferation and cardiac repair. Cell Res. 2017 Aug;27(8):1002-1019.

Yang K, Long Q, Saja K, Huang F, Pogwizd SM, Zhou L, Nakamura J, Yoshida M, and Yang Q*: knockout of the ATPAse inhibitory factor 1 protects the heart from pressure overload-induced cardiac hypertrophy. Sci Rep. 2017 Sep 5;7(1):10501.

Huang L, Zhang K, Guo Y, Huang F, Yang K, Huang K, Zhang F, Long Q*, Yang Q*. Honokiol protects doxorubicin cardiotoxicity via improving mitochondrial function in mouse hearts. Sci Rep. 2017 Sep 20;7(1):11989.

**Corresponding and Co-corresponding author