Tamer M. Mohamed, Ph.D.

Associate Professor of Medicine

Department of Medicine, Division of Cardiovascular Medicine


E-mail 502-852-8428

Education and Training

Ph.D.: University of Manchester, Cardiovascular and Molecular Medicine
Postdoctoral Fellowship: University of Manchester; Gladstone Institutes, Cardiology


Research Interests

My main research interest is to identify novel therapies for heart failure focusing on endogenous heart repair and regeneration mechanisms. As a pharmacist by training and the unique combination of academic and industry experience, my major aim is to perform translational research which directly benefits heart failure patients.

During my research endeavors, I have studied novel mechanisms and therapies for cardiac hypertrophy and heart failure in animal models. During my doctoral and first postdoctoral training, I identified the role of the plasma membrane calcium ATPase isoform 4 (PMCA4) in cardiac physiology and pathophysiology.

As a pharmacist, I have a special interest in translating my findings into human drug therapies for heart disease. Thus, I started screening drugs to identify the first specific inhibitor for PMCA4, which could then be used as a novel treatment for cardiac hypertrophy and heart failure. Recently, in collaboration with the Fraunhofer Institute in Germany, the Medical Research Council in the UK, and the drug company Astra Zeneca, we created a program to identify new drugs that treat heart failure by targeting PMCA4.

To expand my expertise in cardiac regeneration, I joined Prof. Deepak Srivastava's laboratory at the Gladstone Institutes in August 2013. In the Srivastava lab I acquired training on cutting-edge technology for direct cardiac reprogramming, and profiling single-cell genomes and epigenomes during the reprogramming process. The skills that I have learned while working with Prof. Srivastava will be invaluable to running my independent laboratory.

I worked on two parallel approaches to induce endogenous heart repair: direct cardiac reprogramming and inducing cardiomyocyte proliferation. Both approaches were highly successful. The direct reprogramming project was highly recognized by our scientific community, as it was awarded a Scientist Development Grant award from the American Heart Association, manuscript was published in Circulationand this work was chosen as finalist at the Louis N. and Arnold M. Katz Basic Science Research Prize for Young Investigators from the AHA in 2016.

In addition, the cardiomyocyte proliferation project was accepted for publication in Cell and awarded the March 22, 2018 issue cover for the journal. In October 2016 Dr. Srivastava has founded a new start up (Tenaya Therapeutics) with $50 million investment from the column group to develop new therapies for heart failure based on my findings. Therefore, I was the first scientist recruited to the company to lead the efforts of direct cardiac reprogramming where I enjoyed the unique industry experience in building a start up from scratch.

In Tenaya I was able to establish novel system for long term culture of human heart slices and efficiently demonstrating direct cardiac reprogramming in such pre-clinical models. In addition, I was able to reduce the number of essential reprogramming factors in human cardiac fibroblasts to 3 essential factors where they are now under pre-clinical testing for in vivo efficiency in large animals (pigs). Due to the quick success in Tenaya, the research and development section ended very soon and now the major focus on scaling up viral manufacturing and filing IND which is away from my interest.

Therefore, I have decided to go back to academia to initiate new discoveries to treat heart failure mainly focusing on understanding the reprogramming process and cell cycle regulation of cardiomyocyte proliferation.


Featured Publications

  • Ruiz-Velasco A, Raja R, Chen X, Ganenthiran H, Kaur N, Alatawi NHO, Miller JM, Abouleisa RRE, Ou Q, Zhao X, Fonseka O, Wang X, Hille SS, Frey N, Wang T, Mohamed TMA, Müller OJ, Cartwright EJ, Liu W. Restored autophagy is protective against PAK3-induced cardiac dysfunction. iScience. 2023 May 26;26(6):106970. doi: 10.1016/j.isci.2023.106970. PMID: 37324527; PMCID: PMC10265534.
  • Salama ABM, Abouleisa RRE, Ou Q, Tang XL, Alhariry N, Hassan S, Gebreil A, Dastagir M, Abdulwali F, Bolli R, Mohamed TMA. Transient gene therapy using cell cycle factors reverses renin-angiotensin-aldosterone system activation in heart failure rat model. Mol Cell Biochem. 2023 Jun;478(6):1245-1250. doi: 10.1007/s11010-022-04590-2. Epub 2022 Oct 25. PMID: 36282351; PMCID: PMC10126184.
  • Ahmed F, Kahlon T, Mohamed TMA, Ghafghazi S, Settles D. Literature Review: Pathophysiology of Heart Failure with Preserved Ejection Fraction. Curr Probl Cardiol. 2023 Apr 20;48(9):101745. doi: 10.1016/j.cpcardiol.2023.101745. Epub ahead of print. PMID: 37087081.
  • Kaur N, Gare SR, Ruiz-Velasco A, Miller JM, Abouleisa RRE, Ou Q, Shen J, Soran H, Mohamed TMA, Liu W. FGF21/FGFR1-β-KL cascade in cardiomyocytes modulates angiogenesis and inflammation under metabolic stress. Heliyon. 2023 Mar 30;9(4):e14952. doi: 10.1016/j.heliyon.2023.e14952. PMID: 37123894; PMCID: PMC10133673.
  • Huang Y, Wang B, Hassounah F, Price SR, Klein J, Mohamed TMA, Wang Y, Park J, Cai H, Zhang X, Wang XH. The impact of senescence on muscle wasting in chronic kidney disease. J Cachexia Sarcopenia Muscle. 2023 Feb;14(1):126-141. doi: 10.1002/jcsm.13112. Epub 2022 Nov 9. PMID: 36351875; PMCID: PMC9891952.
  • Miller JM, Meki MH, Elnakib A, Ou Q, Abouleisa RRE, Tang XL, Salama ABM, Gebreil A, Lin C, Abdeltawab H, Khalifa F, Hill BG, Abi-Gerges N, Bolli R, El-Baz AS, Giridharan GA, Mohamed TMA. Biomimetic cardiac tissue culture model (CTCM) to emulate cardiac physiology and pathophysiology ex vivo. Commun Biol. 2022 Sep 9;5(1):934. doi: 10.1038/s42003-022-03919-3. PMID: 36085302; PMCID: PMC9463130.
  • Mohamed TMA, Abouleisa R, Hill BG. Metabolic Determinants of Cardiomyocyte Proliferation. Stem Cells. 2022 May 27;40(5):458-467. doi: 10.1093/stmcls/sxac016. PMID: 35263763; PMCID: PMC9156555.
  • Abouleisa RRE, Salama ABM, Ou Q, Tang XL, Solanki M, Guo Y, Nong Y, McNally L, Lorkiewicz PK, Kassem KM, Ahern BM, Choudhary K, Thomas R, Huang Y, Juhardeen HR, Siddique A, Ifthikar Z, Hammad SK, Elbaz AS, Ivey KN, Conklin DJ, Satin J, Hill BG, Srivastava D, Bolli R, Mohamed TMA. Transient Cell Cycle Induction in Cardiomyocytes to Treat Subacute Ischemic Heart Failure. Circulation. 2022 Apr 26;145(17):1339-1355. doi: 10.1161/CIRCULATIONAHA.121.057641. Epub 2022 Jan 21. PMID: 35061545; PMCID: PMC9038650.
  • Kaur N, Ruiz-Velasco A, Raja R, Howell G, Miller JM, Abouleisa RRE, Ou Q, Mace K, Hille SS, Frey N, Binder P, Smith CP, Fachim H, Soran H, Swanton E, Mohamed TMA, Müller OJ, Wang X, Chernoff J, Cartwright EJ, Liu W. Paracrine signal emanating from stressed cardiomyocytes aggravates inflammatory microenvironment in diabetic cardiomyopathy. iScience. 2022 Feb 23;25(3):103973. doi: 10.1016/j.isci.2022.103973. PMID: 35281739; PMCID: PMC8905320.
  • Abdeltawab H, Khalifa F, Hammouda K, Miller JM, Meki MM, Ou Q, El-Baz A, Mohamed TMA. Artificial Intelligence Based Framework to Quantify the Cardiomyocyte Structural Integrity in Heart Slices. Cardiovasc Eng Technol. 2022 Feb;13(1):170-180. doi: 10.1007/s13239-021-00571-6. Epub 2021 Aug 16. PMID: 34402037; PMCID: PMC8847536.