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Titolo:
REGULATION OF CONTRACTILE PROTEINS IN DIABETIC HEART
Autore:
MALHOTRA A; SANGHI V;
Indirizzi:
YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,DIV CARDIOL,1300 MORRIS PK AVE BRONX NY 10461
Titolo Testata:
Cardiovascular Research
fascicolo: 1, volume: 34, anno: 1997,
pagine: 34 - 40
SICI:
0008-6363(1997)34:1<34:ROCPID>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC TROPONIN-I; MYOSIN ATPASE ACTIVITY; ACTOMYOSIN MGATPASE ACTIVITY; LEFT-VENTRICULAR FUNCTION; KINASE-C PHOSPHORYLATION; CA2+-STIMULATED MGATPASE; RECONSTITUTED ACTOMYOSIN; HAMSTER CARDIOMYOPATHY; ISOENZYME DISTRIBUTION; SHORTENING VELOCITY;
Keywords:
DIABETES; CONTRACTILE PROTEINS; MYOSIN ATPASE; TROPONIN; CONTRACTILE FUNCTION; CALCIUM SENSITIVITY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
71
Recensione:
Indirizzi per estratti:
Citazione:
A. Malhotra e V. Sanghi, "REGULATION OF CONTRACTILE PROTEINS IN DIABETIC HEART", Cardiovascular Research, 34(1), 1997, pp. 34-40

Abstract

Diabetes is one of the most prevalent chronic conditions that has a high association with death from cardiovascular disease(sf. An impairedcardiac function independent of vascular disease suggests the existence of a primary myocardial defect in diabetes mellitus, We and others have documented that myocardial performance is impaired in the hearts of chronically diabetic rats and rabbits. Abnormalities in the contractile proteins and regulatory proteins could be responsible for the mechanical defects in streptozotocin (STZ)-diabetic hearts. The major focus of research on contractile proteins in the diabetic state has been on myosin ATPase and its isoenzymes. However, in the contractile protein system, this could be only one of the mechanisms that might be a controlling factor in myofilament contraction in diabetes, To define therole of cardiac contractile as well as regulatory proteins (troponin-tropomyosin) as a whole in the regulation of actomyosin system in diabetic cardiomyopathy, individual proteins of the cardiac system were reconstituted under controlled conditions. Enzymatic data confirmed a diminished calcium sensitivity in the regulation of the cardiac actomyosin system when regulatory protein(s) complex was recombined from diabetic hearts. This diminished calcium sensitivity along with shifts in cardiac myosin heavy chain (V1 --> V3) could contribute to the impairedcardiac function in the hearts of chronic diabetic rats. It has also been reported that sarcomeric proteins such as myosin light chain-2 (MLC-2) and troponin I(TnI) could be involved in regulating muscle contraction and in calcium sensitivity. Since phosphorylation of cardiac TnI is associated with altered maximum enzymatic activity and calcium force relationship in isolated muscle preparations, TnI phosphorylation could contribute to depressed myocardial contractility in experimentaldiabetes, While we have yet to understand the exact function of each component in cardiac muscle and their behavior in concert where all ofthem act in tandem, we have focussed on the role of contractile proteins and their regulation in diabetes in this review. We have also included a brief discussion on other relevant intracellular components, Insummary, there is substantial evidence to suggest that there are independent processes associated with diabetes which effect cardiac performance in experimental animals and in man. The focus of this review hasbeen the explication of a biochemical defect which underlies cardiac contractile dysfunction in experimental models of diabetes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 10:09:05