A Look Between the Cardiomyocytes: The Extracellular Matrix in Heart Failure

Miner, Edward C.; Miller, Wayne L.
January 2006
Mayo Clinic Proceedings;Jan2006, Vol. 81 Issue 1, p71
Academic Journal
The extracellular matrix (ECM) of the heart dynamically interacts with various cellular components of the myocardium, including the myocytes and connective tissue cells. With the development and progression of heart failure, left ventricular (LV) myocardial remodeling occurs. The progression of LV remodeling is accompanied by alterations In the structure and function of the ECM that occur after injury resulting from neurohormonal activation, changes in LV loading conditions, and alterations in myocardial perfusion and metabolism and Is secondary to a host of nonmyocyte signaling pathways that affect repair and remodeling of the myocardium as a whole. This article attempts to review some of these processes and their Interactions and to provide a focus to the often overlooked contribution of the ECM to the development and progression of heart failure and thereby Its potential role as a target for therapy for heart failure.


Related Articles

  • Emerging concepts in cardiac matrix biology. Espira, Leon; Czubryt, Michael P. // Canadian Journal of Physiology & Pharmacology;Dec2009, Vol. 87 Issue 12, p996 

    The cardiac extracellular matrix, far from being merely a static support structure for the heart, is now recognized to play central roles in cardiac development, morphology, and cell signaling. Recent studies have better shaped our understanding of the tremendous complexity of this active and...

  • Gingival Fibroblasts Display Reduced Adhesion and Spreading on Extracellular Matrix: A Possible Basis for Scarless Tissue Repair? Guo, Fen; Carter, David E.; Mukhopadhyay, Anuradha; Leask, Andrew // PLoS ONE;2011, Vol. 6 Issue 11, p1 

    Unlike skin, oral gingiva do not scar in response to injury. The basis of this difference is likely to be revealed by comparing the responses of dermal and gingival fibroblasts to fibrogenic stimuli. Previously, we showed that, compared to dermal fibroblasts, gingival fibroblasts are less...

  • Cardiac muscle cell cytoskeletal protein 4.1: Analysis of transcripts and subcellular location-relevance to membrane integrity, microstructure, and possible role in heart failure. Taylor-Harris, Pamela M.; Keating, Lisa A.; Maggs, Alison M.; Phillips, Gareth W.; Birks, Emma J.; Franklin, Rodney C. G.; Yacoub, Magdi H.; Baines, Anthony J.; Pinder, Jennifer C. // Mammalian Genome;Mar2005, Vol. 16 Issue 3, p137 

    The spectrin-based cytoskeleton assembly has emerged as a major player in heart functioning; however, cardiac protein 4.1, a key constituent, is uncharacterized. Protein 4.1 evolved to protect cell membranes against mechanical stresses and to organize membrane microstructure. 4.1 Proteins are...

  • Effects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: reversal of increased β-myosin heavy chain gene expression. Wang, Baohua; Ouyang, Jingping; Xia, Zhengyuan // Canadian Journal of Physiology & Pharmacology;Aug/Sep2006, Vol. 84 Issue 8/9, p935 

    Thyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased α-myosin heavy chain (α-MHC, the high ATPase activity isoform) expression. In contrast, angiotensin II (Ang II) induces an...

  • Mending a Broken Heart: Bioengineered Patches and Scaffolds for Cardiac Repair. Ballard, Victoria L. T. // Recent Patents on Biomedical Engineering;Jun2010, Vol. 3 Issue 2, p107 

    Cardiovascular disease is the leading cause of morbidity and mortality in the United States, accounting for more than one third of all deaths. In heart failure patients, progressive impairment in the ability of the heart to effectively pump blood to the body is caused by adverse remodeling, scar...

  • Perfusion-decellularized matrix: using nature's platform to engineer a bioartificial heart. Ott, Harald C.; Matthiesen, Thomas S.; Goh, Saik-Kia; Black, Lauren D.; Kren, Stefan M.; Netoff, Theoden I.; Taylor, Doris A. // Nature Medicine;Feb2008, Vol. 14 Issue 2, p213 

    About 3,000 individuals in the United States are awaiting a donor heart; worldwide, 22 million individuals are living with heart failure. A bioartificial heart is a theoretical alternative to transplantation or mechanical left ventricular support. Generating a bioartificial heart requires...

  • Intracellular devastation in heart failure. Federica del Monte; Roger Hajjar // Heart Failure Reviews;Jun2008, Vol. 13 Issue 2, p151 

    Abstract  End-stage heart failure is characterized by a number of abnormalities at the cellular level, which include changes in excitation–contraction coupling, alterations in contractile proteins and activation/deactivation of signaling pathways. Even though many of...

  • Molecular mechanisms of cardiomyogenesis and the prospects for cardiomyocyte regeneration in cardiac failure. Shirinsky, V. P.; Khapchaev, A. Yu.; Stepanova, O. V. // Molecular Biology;Sep2008, Vol. 42 Issue 5, p762 

    The review briefs the current state of research in molecular biological and cell aspects of cardiac development and the prospects of applying the corresponding results to treating heart failure by cardiomyocyte regeneration in damaged myocardium.

  • Differential activation of matrix metalloproteinases in heart failure with and without ventricular dilatation Nishikawa, Nagahiro; Yamamoto, Kazuhiro; Sakata, Yasushi; Mano, Toshiaki; Yoshida, Junichi; Miwa, Takeshi; Takeda, Hiroshi; Hori, Masatsugu; Masuyama, Tohru // Cardiovascular Research;Mar2003, Vol. 57 Issue 3, p766 

    Objective: Remodeling of extracellular matrix (ECM) is considered to contribute to progression of left ventricular (LV) remodeling and matrix metalloproteinases (MMPs) play crucial roles in regulation of ECM. Activation of MMPs is observed in systolic heart failure (SHF) and is suggested...


Read the Article


Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics