Tufts Medical Center
800 Washington St.
Boston, MA 02111
Phone #: 617-636-8066
Fax #: 617-636-7175
2014, Paper of the Year, Inhalation & Respiratory Specialty Section, Society of Toxicology
Maron BJ, Rowin EJ, Arkun K, Rastegar H, Larson AM, Maron MS and Chin MT. Adult monozygotic twins with hypertrophic cardiomyopathy and identical disease expression and clinical course. Am J Cardiol 2020 doi: 10.1016/j.amjcard.2020.04.020. Epub 2020 Apr 23.
Larson A, Libermann TA, Bowditch H, Das G, Diakos N, Huggins GS, Rastegar H, Chen FY, Rowin EJ, Maron MS, Chin MT. Plasma Proteomic Profiling in Hypertrophic Cardiomyopathy Patients before and after Surgical Myectomy Reveals Post-Procedural Reduction in Systemic Inflammation. Int J Mol Sci. 2021 Mar 1;22(5):2474. doi: 10.3390/ijms22052474. PMID: 33804404; PMCID: PMC7957543.
Chou C, Chin MT. Pathogenic Mechanisms of Hypertrophic Cardiomyopathy beyond Sarcomere Dysfunction. International Journal of Molecular Sciences. 2021;22(16):8933. PubMed PMID: doi:10.3390/ijms22168933.
Wolter NL, LeClair MJ, Chin MT. Plasma metabolomic profiling of hypertrophic cardiomyopathy patients before and after surgical myectomy suggests postoperative improvement in metabolic function. BMC Cardiovasc Disord. 2021;21(1):617. Epub 2021/12/29. doi: 10.1186/s12872-021-02437-0. PubMed PMID: 34961475.
Codden CJ, Chin MT. Common and Distinctive Intercellular Communication Patterns in Human Obstructive and Nonobstructive Hypertrophic Cardiomyopathy. Int J Mol Sci. 2022 Jan 15;23(2). doi: 10.3390/ijms23020946. PubMed PMID: 35055131; PubMed Central PMCID: PMC8780670.
Larson A, Codden CJ, Huggins GS, Rastegar H, Chen FY, Maron BJ, Rowin EJ, Maron MS, Chin MT. Altered intercellular communication and extracellular matrix signaling as a potential disease mechanism in human hypertrophic cardiomyopathy. Sci Rep. 2022 Mar 25;12(1):5211. doi: 10.1038/s41598-022-08561-x. PubMed
Chin MT, Maemura KM, Fukumoto S, Jain MK, Layne MD, Watanabe M, Hsieh C-M and Lee M-E. Cardiovascular basic helix-loop-helix factor-1, a novel transcriptional repressor expressed preferentially in the developing and adult cardiovascular system. J. Biol. Chem. 2000; 275: 6381-6387.
Sakata Y, Kamei CN, Nakagami H, Bronson R, Liao JK and Chin MT. Ventricular septal defects and cardiomyopathy in mice lacking the transcription factor CHF1/Hey2. Proc. Natl. Acad. Sci. USA 2002; 99: 16197-16202.
Sakata Y, Xiang F, Chen Z, Kiriyama Y, Kamei CN, Simon DI and Chin MT. Transcription factor CHF1/Hey2 regulates neointimal formation in vivo and vascular smooth muscle proliferation and migration in vitro. Arterioscler Thromb Vasc Biol 2004; 24: 2069-2074.
Koibuchi N and Chin MT. CHF1/Hey2 plays a pivotal role in left ventricular maturation through suppression of ectopic atrial gene expression. Circ. Res. 2007; 100: 850-855.
Weldy CS, Liu Y, Chang Y-C, Medvedev IO, Fox JR, Larson TV, Chien W-M, Chin MT. In utero and early life exposure to diesel exhaust air pollution increases adult susceptibility to heart failure in mice. Part Fibre Toxicol. 2013, 10:59.
Weldy CS, Liu Y, Liggitt HD, Chin MT. In utero exposure to diesel exhaust air pollution promotes adverse intrauterine conditions, resulting in weight gain, altered blood pressure, and increased susceptibility to heart failure in adult mice. PLoS One 2014; 9:e88582.
Hartman ME, Librande JR, Medvedev IO, Ahmad RN, Moussavi-Harami F, Gupta PP, Chien W-M, Chin MT. An Optimized System of Mouse Embryonic Stem Cell Cardiac Differentiation for the Assessment of Differentiation Modifiers. PLoS One 2014; 9:e93033.
Hartman ME, Liu Y, Zhu W-Z, Chien W-M, Weldy CS, Fishman GI, Laflamme MA, Chin MT. Myocardial deletion of transcription factor CHF1/Hey2 results in altered myocyte action potential and mild conduction system expansion but does not alter conduction system function or promote spontaneous arrhythmias. FASEB J. 2014; 28: 3007-3015.
Chien W-M, Liu Y, Chin MT. Genomic DNA Recombination with Cell-Penetrating Peptide-Tagged Cre Protein in Mouse Skeletal and Cardiac Muscle. Genesis 2014; 52: 695-701.
*Goodson JM, Weldy CS, MacDonald JW, Liu Y, Bammler TK, Chien W-M, and Chin MT. In utero exposure to diesel exhaust particulates is associated with an altered cardiac transcriptional response to transverse aortic constriction and altered DNA methylation. FASEB J. 2017 Jul 27. pii: fj.201700032R. doi: 10.1096/fj.201700032R. [Epub ahead of print] PMID:28751527.
Michael T. Chin, MD, PhD is the Research Director of the Hypertrophic Cardiomyopathy (HCM) Center and Research Institute at Tufts Medical Center and a Principal Investigator in the Molecular Cardiology Research Institute (MCRI). In his role as the HCM Research Director, Dr. Chin identifies basic pathways influencing the development of hypertrophy and fibrosis and the attendant electrical instability, with the goals of illuminating potential new treatment paradigms and drug targets for HCM. In the MCRI, Dr. Chin investigates mechanisms and treatments for other genetic causes of heart failure and exploring epigenetic mechanisms by which air pollution causes cardiac failure.
Dr. Chin is trained as a virologist, molecular biologist, biochemist and a cardiologist, studying the molecular biology of the cardiovascular system while also caring for patients. His research interest is in understanding the genetic basis of cardiovascular disease, with a focus on how regulation of gene expression affects cardiovascular disease phenotypes, with a goal to develop therapeutic agents that can ameliorate pathological phenotypes and thus provide treatments for cardiovascular diseases. The activities of the Chin Lab include developing an enzyme replacement therapy for a genetic cardiomyopathy disorder, Barth Syndrome, and identifying molecular pathways that regulate cardiac sensitivity to developmental diesel exhaust exposure. His lab also has expertise in analyzing developmental phenotypes in genetically modified mice, differentiating embryonic stem cells to cardiomyocytes, culturing primary vascular, cardiac and embryonic cells for gain and loss of function studies and also in assessing for cardiac hypertrophy and heart failure in vitro and in vivo, as well as experience in measuring mitochondrial respiration, skeletal muscle contraction and mouse treadmill exercise performance.
Dr. Chin completed medical school and a PhD at the University of Rochester. He then went on to do a residency at The Johns Hopkins Hospital, a post-doctoral research fellowship at the National Institute on Aging, and a fellowship in Cardiovascular Diseases at Brigham and Women’s Hospital. Dr. Chin is a member of the American Society for Clinical Investigation and of the Editorial Board for the Journal of Molecular and Cellular Cardiology. He has served on NIH and AHA Study Sections and has received awards for his work at every stage of his career.
American College of Cardiology
American College of Physicians
American Heart Association
American Physiological Society
American Society for Biochemistry and Molecular Biology
American Society for Clinical Investigation
International Society for Heart Research
Dr. Chin is trained as a virologist, molecular biologist, biochemist and a cardiologist, and has studied the molecular biology of the cardiovascular system and cared for patients for many years. His general interest is in understanding the genetic basis of cardiovascular disease, with a focused interest on how regulation of gene expression affects cardiovascular disease phenotypes. Within this context, his goal is to develop therapeutic agents that can ameliorate pathological phenotypes and thus provide treatments for cardiovascular diseases. His lab’s current activities include developing an enzyme replacement therapy for a genetic cardiomyopathy disorder, Barth Syndrome, identifying molecular pathways that regulate cardiac sensitivity to developmental diesel exhaust exposure, and understanding the pathogenesis of hypertrophic cardiomyopathy. In his previous work he was among the first to identify and characterize a bHLH transcription factor, CHF1/Hey2, which regulates the development of the myocardium, atrioventricular valves, interventricular septum and coronary vasculature. His lab has expertise in analyzing developmental phenotypes in genetically modified mice, differentiating embryonic stem cells to cardiomyocytes, culturing primary vascular, cardiac and embryonic cells for gain and loss of function studies and also in assessing for cardiac hypertrophy and heart failure in vitro and in vivo. He also has extensive experience expressing and purifying proteins containing cellular penetrating peptide tags for use in protein therapy. He also experience in measuring mitochondrial respiration, skeletal muscle contraction and mouse treadmill exercise performance. These broad areas of expertise in cardiovascular investigation provide versatility for analysis of today’s cardiovascular problems and development of tomorrow’s cardiovascular therapies.