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Titolo:
Plasticity in skeletal cardiac, and smooth muscle - Invited review: Pathophysiology of cardiac muscle contraction and relaxation as a result of alterations in thin filament regulation
Autore:
Hernandez, OM; Housmans, PR; Potter, JD;
Indirizzi:
Univ Miami, Sch Med, Dept Mol & Cellular Pharmacol, Miami, FL 33136 USA Univ Miami Miami FL USA 33136 l & Cellular Pharmacol, Miami, FL 33136 USA Mayo Clin & Mayo Fdn, Dept Anesthesiol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 siol, Rochester, MN 55905 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 3, volume: 90, anno: 2001,
pagine: 1125 - 1136
SICI:
8750-7587(200103)90:3<1125:PISCAS>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; TROPONIN-T MUTATIONS; ALPHA-TROPOMYOSIN GENE; HEAVY-CHAIN GENE; MISSENSE MUTATION; FUNCTIONAL CONSEQUENCES; TRANSGENIC MICE; I GENE; CLINICAL-FEATURES; DELETION MUTATION;
Keywords:
familial hypertrophic cardiomyopathy; troponin; tropomyosin; actin; myocardium;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
100
Recensione:
Indirizzi per estratti:
Indirizzo: Potter, JD Univ Miami, Sch Med, Dept Mol & Cellular Pharmacol, 1600 NW 10th Ave, Miami, FL 33136 USA Univ Miami 1600 NW 10th Ave Miami FL USA 33136 mi, FL 33136 USA
Citazione:
O.M. Hernandez et al., "Plasticity in skeletal cardiac, and smooth muscle - Invited review: Pathophysiology of cardiac muscle contraction and relaxation as a result of alterations in thin filament regulation", J APP PHYSL, 90(3), 2001, pp. 1125-1136

Abstract

Invited Review: Pathophysiology of cardiac muscle contraction and relaxation as a result of alterations in thin filament regulation. J Appl Physiol 90: 1125-1136, 2001.-Cardiac muscle contraction depends on the tightly regulated interactions of thin and thick filament proteins of the contractile apparatus. Mutations of thin filament proteins (actin, tropomyosin, and troponin), causing familial hypertrophic cardiomyopathy (FHC), occur predominantly in evolutionarily conserved regions and induce various functional defects that impair the normal contractile mechanism. Dysfunctional properties observed with the FHC mutants include altered Ca2+ sensitivity, changes in ATPase activity, changes in the force and velocity of contraction, and destabilization of the contractile complex. One apparent tendency observed in these thin filament mutations is an increase in the Ca2+ sensitivity of force development. This trend in Ca2+ sensitivity is probably induced by alteringthe cross-bridge kinetics and the Ca2+ affinity of troponin C. These in vitro defects lead to a wide variety of in vivo cardiac abnormalities and phenotypes, some more severe than others and some resulting in sudden cardiac death.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 22:14:50