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Front Physiol. 2017 Aug 30;8:631. doi: 10.3389/fphys.2017.00631. eCollection 2017.

Increased Hemodynamic Load in Early Embryonic Stages Alters Myofibril and Mitochondrial Organization in the Myocardium.

Frontiers in physiology

Madeline Midgett, Claudia S López, Larry David, Alina Maloyan, Sandra Rugonyi

Affiliations

  1. Biomedical Engineering, Oregon Health & Science UniversityPortland, OR, United States.
  2. Multiscale Microscopy Core, OHSU Center for Spatial Systems Biomedicine, Oregon Health & Science UniversityPortland, OR, United States.
  3. Proteomics Core, Oregon Health & Science UniversityPortland, OR, United States.
  4. Knight Cardiovascular Institute, Oregon Health & Science UniversityPortland, OR, United States.

PMID: 28912723 PMCID: PMC5582297 DOI: 10.3389/fphys.2017.00631

Abstract

Normal blood flow is essential for proper heart formation during embryonic development, as abnormal hemodynamic load (blood pressure and shear stress) results in cardiac defects seen in congenital heart disease (CHD). However, the detrimental remodeling processes that relate altered blood flow to cardiac malformation and defects remain unclear. Heart development is a finely orchestrated process with rapid transformations that occur at the tissue, cell, and subcellular levels. Myocardial cells play an essential role in cardiac tissue maturation by aligning in the direction of stretch and increasing the number of contractile units as hemodynamic load increases throughout development. This study elucidates the early effects of altered blood flow on myofibril and mitochondrial configuration in the outflow tract myocardium

Keywords: cardiac development; congenital heart disease; embryonic myocardial maturation; hemodynamic regulation of heart development; hemodynamically-induced cardiac remodeling; outflow tract development

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