Matthew J Wolf

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Primary Appointment

Associate Professor, Medicine- Cardiovascular Medicine

Education

  • Fellowship, Cardiology, Duke University School of Medicine, Durham, NC
  • Residency, Internal Medicine, Duke University School of Medicine, Durham, NC
  • MD, Washington University School of Medicine
  • PhD, Biochemistry, Washington University School of Medicine

Research Disciplines

Cardiovascular Biology, Genetics, Physiology

Research Interests

Identification of genes and pathways that cause or modify cardiac hypertrophy and heart failure.

Research Description

Our mission is to understand how signaling molecules mediate cardiomyocyte growth, hypertrophy, and heart failure. We use novel approaches based on fruit fly genetics to identify genes that cause or modify cardiomyopathies and translate these findings using mammalian cell-based systems and transgenic mice. Our multidisciplinary approach employs state-of-the-art Optical Coherence Tomography, confocal microscopy, molecular and cell biology, proteomics, and physiology to understand cardiovascular disease.

Personal Statement

The Wolf lab in the Robert M. Berne Cardiovascular Research Center at UVA focuses on the development of new therapeutics to treat cardiovascular diseases. Our mission is to better understand the signals mediating cardiomyocyte growth, hypertrophy, and heart failure. The mammalian heart has little, if any, ability to generate new cardiomyocytes after injury, and identifying cycling cells is challenging. We develop sophisticated transgenic mice to label and genetically manipulate adult cycling cardiomyocytes and use a variety of disease models to investigate cardiac regeneration. Our work has identified new therapeutics that improve myocardial function after injury. Additionally, we use cardiac MRI to investigate the mechanisms causing microvascular coronary disease and impaired myocardial perfusion reserve in models of diet-induced obesity.

Training

  • Basic Cardiovascular Research Training Grant

Selected Publications

2024

Pavelec, C. M., Young, A. P., Luviano, H. L., Orrell, E. E., Szagdaj, A., Poudel, N., . . . Leitinger, N. (2024). Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy. CIRCULATION RESEARCH, 135(4), 503-517. doi:10.1161/CIRCRESAHA.124.324650

Pavelec, C. M., Young, A. P., Luviano, H. L., Orrell, E. E., Szagdaj, A., Poudel, N., . . . Leitinger, N. (2024). Pannexin 1 Channels Control Cardiomyocyte Metabolism and Neutrophil Recruitment During Non-Ischemic Heart Failure.. bioRxiv. doi:10.1101/2023.12.29.573679

Cochran, J. D., Leathers, T. A., Maldosevic, E., Siejda, K. W., Vitello, J., Lee, H., . . . Wolf, M. J. (2024). Cell cycle specific, differentially tagged ribosomal proteins to measure phase specific transcriptomes from asynchronously cycling cells. SCIENTIFIC REPORTS, 14(1). doi:10.1038/s41598-024-52085-5

Woo, L. A., Wintruba, K. L., Wissmann, B., Tkachenko, S., Kubicka, E., Farber, E., . . . Saucerman, J. J. (2024). Multi-omic analysis reveals VEGFR2, PI3K, and JNK mediate the small molecule induction of human iPSC-derived cardiomyocyte proliferation. ISCIENCE, 27(8). doi:10.1016/j.isci.2024.110485

2023

Chakraborty, A., Peterson, N. G., King, J. S., Gross, R. T., Pla, M. M., Thennavan, A., . . . Fox, D. T. (2023). Conserved chamber-specific polyploidy maintains heart function in Drosophila. DEVELOPMENT, 150(16). doi:10.1242/dev.201896

Bazgir, F., Nau, J., Nakhaei-Rad, S., Amin, E., Wolf, M. J., Saucerman, J. J., . . . Ahmadian, M. R. (2023). The Microenvironment of the Pathogenesis of Cardiac Hypertrophy. CELLS, 12(13). doi:10.3390/cells12131780

Nakhaei-Rad, S., Haghighi, F., Bazgir, F., Dahlmann, J., Busley, A. V., Buchholzer, M., . . . Ahmadian, M. R. (2023). Molecular and cellular evidence for the impact of a hypertrophic cardiomyopathy-associated RAF1 variant on the structure and function of contractile machinery in bioartificial cardiac tissues. COMMUNICATIONS BIOLOGY, 6(1). doi:10.1038/s42003-023-05013-8

Shah, S. A., Reagan, C. E., Bresticker, J. E., Wolpe, A. G., Good, M. E., Macal, E. H., . . . Epstein, F. H. (2023). Obesity-Induced Coronary Microvascular Disease Is Prevented by iNOS Deletion and Reversed by iNOS Inhibition. JACC-BASIC TO TRANSLATIONAL SCIENCE, 8(5), 501-514. doi:10.1016/j.jacbts.2022.11.005

2022

Fischer, J. A., Monroe, T. O., Pesce, L. L., Sawicki, K. T., Quattrocelli, M., Bauer, R., . . . McNally, E. M. (2023). Opposing effects of genetic variation in MTCH2 for obesity versus heart failure. HUMAN MOLECULAR GENETICS, 32(1), 15-29. doi:10.1093/hmg/ddac176

Shah, S. A., Echols, J. T., Sun, C., Wolf, M. J., & Epstein, F. H. (2022). Accelerated fatty acid composition MRI of epicardial adipose tissue: Development and application to eplerenone treatment in a mouse model of obesity-induced coronary microvascular disease. MAGNETIC RESONANCE IN MEDICINE, 88(4), 1734-1747. doi:10.1002/mrm.29348

Pavelce, C. M., Wolf, M., Yeudall, S., Upchurch, C., & Leitinger, N. (2022). A Critical Role for Pannexin 1 in Heart Failure Induced by Acute and Chronic Isoproterenol Administration. FASEB JOURNAL, 36. doi:10.1096/fasebj.2022.36.S1.L7728

Young, A., Bradley, L. A., Farrar, E., Bilcheck, H. O., Tkachenko, S., Saucerman, J. J., . . . Wolf, M. J. (2022). Inhibition of DYRK1a Enhances Cardiomyocyte Cycling After Myocardial Infarction. CIRCULATION RESEARCH, 130(9), 1345-1361. doi:10.1161/CIRCRESAHA.121.320005

Young, A., Bradley, L. A., & Wolf, M. J. (2022). In Vivo Methods to Monitor Cardiomyocyte Proliferation. JOURNAL OF CARDIOVASCULAR DEVELOPMENT AND DISEASE, 9(3). doi:10.3390/jcdd9030073

2021

Drake, J. C., Wilson, R. J., Laker, R. C., Guan, Y., Spaulding, H. R., Nichenko, A. S., . . . Yan, Z. (2021). Mitochondria-localized AMPK responds to local energetics and contributes to exercise and energetic stress-induced mitophagy. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 118(37). doi:10.1073/pnas.2025932118

Good, M. E., Young, A. P., Wolpe, A. G., Ma, M., Hall, P. J., Duffy, C. K., . . . Isakson, B. E. (2021). Endothelial Pannexin 1 Regulates Cardiac Response to Myocardial Infarction. CIRCULATION RESEARCH, 128(8), 1211-1213. doi:10.1161/CIRCRESAHA.120.317272

2020

Bradley, L. A., Young, A., Li, H., Billcheck, H. O., & Wolf, M. J. (2021). Loss of Endogenously Cycling Adult Cardiomyocytes Worsens Myocardial Function. CIRCULATION RESEARCH, 128(2), 155-168. doi:10.1161/CIRCRESAHA.120.318277

Petersen, C. E., Wolf, M. J., & Smyth, J. T. (2020). Suppression of store-operated calcium entry causes dilated cardiomyopathy of the Drosophila heart. BIOLOGY OPEN, 9(3). doi:10.1242/bio.049999

Petersen, C. E., Wolf, M. J., & Smyth, J. T. (2020). Suppression of store-operated calcium entry causes dilated cardiomyopathy of the Drosophila heart.. Biology open. doi:10.1242/bio.049999

2019

Cresci, S., Pereira, N. L., Ahmad, F., Byku, M., de las Fuentes, L., Lanfear, D. E., . . . Wolf, M. J. (2019). Heart Failure in the Era of Precision Medicine: A Scientific Statement From the American Heart Association. CIRCULATION-GENOMIC AND PRECISION MEDICINE, 12(10), 458-485. doi:10.1161/HCG.0000000000000058

2018

Woo, L. A., Tkachenko, S., Ding, M., Plowright, A. T., Engkvist, O., Andersson, H., . . . Saucerman, J. J. (2019). High-content phenotypic assay for proliferation of human iPSC-derived cardiomyocytes identifies L-type calcium channels as targets. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 127, 204-214. doi:10.1016/j.yjmcc.2018.12.015

Abraham, D. M., Lee, T. E., Watson, L. J., Mao, L., Chandok, G., Wang, H. -G., . . . Rockman, H. A. (2018). The two-pore domain potassium channel TREK-1 mediates cardiac fibrosis and diastolic dysfunction. JOURNAL OF CLINICAL INVESTIGATION, 128(11), 4843-4855. doi:10.1172/JCI95945

Wolf, M. J. (2018). "HETE"ing up mitochondria in human heart failure. JOURNAL OF BIOLOGICAL CHEMISTRY, 293(1), 130-131. doi:10.1074/jbc.H117.001021

2016

Wolf, M. J. (2016). SPARCling Study of a Drosophila Cardiomyopathy. CIRCULATION-CARDIOVASCULAR GENETICS, 9(2), 104-106. doi:10.1161/CIRCGENETICS.116.001394

Wolf, M. J., Noeth, D., Rammohan, C., & Shah, S. H. (2016). Complexities of Genetic Testing in Familial Dilated Cardiomyopathy. CIRCULATION-CARDIOVASCULAR GENETICS, 9(1), 95-99. doi:10.1161/CIRCGENETICS.115.001157

2015

Gao, Q. Q., Wyatt, E., Goldstein, J. A., LoPresti, P., Castillo, L. M., Gazda, A., . . . McNally, E. M. (2015). Reengineering a transmembrane protein to treat muscular dystrophy using exon skipping. JOURNAL OF CLINICAL INVESTIGATION, 125(11), 4186-4195. doi:10.1172/JCI82768

Hardy, C. M., Birse, R. T., Wolf, M. J., Yu, L., Bodmer, R., & Gibbs, A. G. (2015). Obesity-associated cardiac dysfunction in starvation-selected Drosophila melanogaster. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 309(6), R658-R667. doi:10.1152/ajpregu.00160.2015

Yu, L., Daniels, J. P., Wu, H., & Wolf, M. J. (2015). Cardiac hypertrophy induced by active Raf depends on Yorkie-mediated transcription. SCIENCE SIGNALING, 8(362). doi:10.1126/scisignal.2005719

2014

Lee, T. E., Yu, L., Wolf, M. J., & Rockman, H. A. (2014). Galactokinase Is a Novel Modifier of Calcineurin-Induced Cardiomyopathy in Drosophila. GENETICS, 198(2), 591-U209. doi:10.1534/genetics.114.166777

2013

Wolf, M. J. (2013). Towards Understanding the Impact of Sarcomeric Gene Mutations. JACC-HEART FAILURE, 1(6), 467-468. doi:10.1016/j.jchf.2013.09.004

Yu, L., Daniels, J., Glaser, A. E., & Wolf, M. J. (2013). Raf-mediated cardiac hypertrophy in adult Drosophila. DISEASE MODELS & MECHANISMS, 6(4), 964-976. doi:10.1242/dmm.011361

Abraham, D. M., & Wolf, M. J. (2013). Disruption of Sarcoendoplasmic Reticulum Calcium ATPase Function in Drosophila Leads to Cardiac Dysfunction. PLOS ONE, 8(10). doi:10.1371/journal.pone.0077785

2012

Wooten, E. C., Hebl, V. B., Wolf, M. J., Greytak, S. R., Orr, N. M., Draper, I., . . . Huggins, G. S. (2013). Formin Homology 2 Domain Containing 3 Variants Associated With Hypertrophic Cardiomyopathy. CIRCULATION-CARDIOVASCULAR GENETICS, 6(1), 10-18. doi:10.1161/CIRCGENETICS.112.965277

Wolf, M. J. (2012). Modeling Dilated Cardiomyopathies in Drosophila. TRENDS IN CARDIOVASCULAR MEDICINE, 22(3), 55-61. doi:10.1016/j.tcm.2012.06.012

Casad, M. E., Yu, L., Daniels, J. P., Wolf, M. J., & Rockman, H. A. (2012). Deletion of Siah-interacting protein gene in Drosophila causes cardiomyopathy. MOLECULAR GENETICS AND GENOMICS, 287(4), 351-360. doi:10.1007/s00438-012-0684-x

2011

Wolf, M. J., & Rockman, H. A. (2011). Drosophila, Genetic Screens, and Cardiac Function. CIRCULATION RESEARCH, 109(7), 794-806. doi:10.1161/CIRCRESAHA.111.244897

Casad, M. E., Abraham, D., Kim, I. -M., Frangakis, S., Dong, B., Lin, N., . . . Rockman, H. A. (2011). Cardiomyopathy Is Associated with Ribosomal Protein Gene Haplo-Insufficiency in Drosophila melanogaster. GENETICS, 189(3), 861-870. doi:10.1534/genetics.111.131482

Lin, N., Badie, N., Yu, L., Abraham, D., Cheng, H., Bursac, N., . . . Wolf, M. J. (2011). A Method to Measure Myocardial Calcium Handling in Adult Drosophila. CIRCULATION RESEARCH, 108(11), 1306-1U37. doi:10.1161/CIRCRESAHA.110.238105

2010

Goldstein, J. A., Kelly, S. M., LoPresti, P. P., Heydemann, A., Earley, J. U., Ferguson, E. L., . . . McNally, E. M. (2011). SMAD signaling drives heart and muscle dysfunction in a Drosophila model of muscular dystrophy. HUMAN MOLECULAR GENETICS, 20(5), 894-904. doi:10.1093/hmg/ddq528

Yu, L., Lee, T., Lin, N., & Wolf, M. J. (2010). Affecting Rhomboid-3 Function Causes a Dilated Heart in Adult Drosophila. PLOS GENETICS, 6(5). doi:10.1371/journal.pgen.1000969

Kim, I. -M., Wolf, M. J., & Rockman, H. A. (2010). Gene Deletion Screen for Cardiomyopathy in Adult Drosophila Identifies a New Notch Ligand. CIRCULATION RESEARCH, 106(7), 1233-U141. doi:10.1161/CIRCRESAHA.109.213785