Title: Cardiac injury of the newborn mammalian heart – current status

Biography:

Soren P Sheikh, Professor of Clinical Biochemistry, Dept. Head, Odense University Hospital, grew up in Denmark and received his Bachelor's degree from the University of Copenhagen in 1985. After he obtained his Ph.D. degree from the University of Copenhagen 1992, he finished his clinical education, and continued his laboratory work with signal transduction of 7 TM receptors & microRNA at Rigshospitalet, Copenhagen. He spend one year as a research associate at University of Michigan in 1989, and was appointed Professor at the University of Copenhagen in 1995. Next, he joined Professor Henry Bourne in San Francisco at the UCSF from 1996-1999. In the meantime, Sheikh finished his specialist-degree in Clinical Biochemistry, and was appointed Head of Department Clinical Biochemistry & Pharmacology, Odense University Hospital (OUH) in 1992, and began investigations of stem cell differentiation and clinical application in erectile dysfunction and lymphedema. Sheikh was appointed Head of Center for Regenerative Medicine at OUH in 2015. He has received various awards and grants, with the most representative being a 4 mio $ (USD) grant from the Danish Innovation Foundation in 2017.

Abstract

Cardiac vascular Disease is the leading cause of death in Europe.  Although many human organs regenerate completely upon partial damage, the adult is a clear exception from this paradigm. Instead myocardial infarction results in scar formation, and therapies for cardiomyocyte regeneration are warranted. Recently, it was suggested that newborn mammals have full capacity for regeneration of their hearts after apical resection. Using novel methods of myocardial function and scarring including F-18-fluorodeoxyglucose positron emission tomography (FDG-PET), we have intensively tested this interesting hypothesis. We have applied multiple injury models and analyzed mammalian hearts at longer time points after injury based on the observation that zebrafish hearts pass through a phase of fibrosis before complete regeneration. In addition, we investigated the possibility that apical resection either inhibits, delays, or reverses cardiomyocyte centrosome disassembly and binucleation. None of the injured hearts exhibited full regeneration but instead exhibited persistent scarring and reduced wall motion. Taken together, our work showed that suggests that a potential regenerative program in the new newborn mammalian heart is less likely to emerge due to developmental mechanisms that induce terminal differentiation of cardiomyocytes.