Mahasweta Girgenrath, PhD

Mahasweta Girgenrath, PhD

Assistant Professor, Department of Health Sciences
Programs in Human Physiology
Director, Muscle Disorders & Regenerative Biology Laboratory
635 Commonwealth Ave
B.Sc. (Biology), Delhi University
B.Ed. (Biology and English), Annamalai University
Ph.D. (Biology), Northeastern University
Website or Lab
Muscle Disorders & Regenerative Biology Laboratory
Download CV

Courses Taught

  • HS 360 Biology of Muscle in Health and Disease
  • HP151 Introduction to Health Professions

Scholarly Interests

My research program uses a combination of molecular, cellular and in vivo techniques to understand the mechanisms that underlie tissue growth, repair, and survival in the context of neuromuscular diseases such as muscular dystrophy. My long-term goal is to translate the findings into the development of effective treatment and cures for damaged or diseased muscle.

Selected Publications

Kumar A, Accorsi A, Rhee Y, Girgenrath M. Do’s and Don’ts in the Preparation of Muscle Cryosections for Histological Analysis. J Vis Exp. 2015 May 15;(99).

Mehuron T, Kumar A, Duarte L, Yamauchi J, Accorsi A, Girgenrath M. Dysregulation of matricellular proteins is an early signature of pathology in laminin-deficient muscular dystrophy. Skelet Muscle. 2014 Jul 2;4:14.

Yamauchi J, Kumar A, Duarte L, Mehuron T, Girgenrath M. Triggering regeneration and tackling apoptosis: a combinatorial approach to treating congenital muscular dystrophy type 1 A. Hum Mol Genet. 2013 Nov 1;22(21):4306-17.

Girgenrath, M., Beermann, M. L, Vishnudas, V., Homma, S. and Miller, J. B. (2008). Pathology is alleviated by doxycycline in a laminin-a2 null model of MDC1A. Annals of Neurology.

Girgenrath, M. Kostek, C. A., Browning, B., Winkles, J. Michaelson, J., Scott, M., Hsu, Y., Flavell, R. A., Miller, J. B., and Linda C and Zheng, T. S. (2006) Regulation of muscle satellite cell activation by Tweak/Fn14 pathway. EMBO J: 17124496.

Miller, J. B. and Girgenrath, M. (2006). Potential usefulness of anti-apoptosis therapy in neuromuscular diseases. Trends Mol. Med. Jun; 12(6): 279-86. Epub 2006 May 2.

Girgenrath, M., Kostek, C. A., and Miller, J. B. (2005). Diseased muscles that lacks dystrophin or laminin-a2 have altered composition and proliferation of mononuclear cell populations. BMC Neurology. 5:7.

Girgenrath, M., Dominov, J. A., Kostek, C. A., and Miller, J. B. (2004) Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy. J Clin Invest 114(11), 1635-9.

Current Research Funding

  • Principle Investigator
    Cure CMD, “Inhibition of Angiotensin II Signaling in Congenital Muscular Dystrophy Type 1A” 2014-2015:
  • Principle Investigator
    National Institute Of health (R21), “A Combinatorial Strategy to Treat Congenital Muscular Dystrophy” 2008-2010
  • Principle Investigator
    Muscular Dystrophy Association, Inc. (Development grant), “A combinatorial approach to treat the pathology” 2007-2009