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001-es BibID:	BIBFORM015745
Első szerző:	Machackova, Jarmila
Cím:	Molecular defects in cardiac myofibrillar proteins due to thyroid hormone imbalance and diabetes / Jarmila Machackova, Barta Judit, Naranjan S. Dhalla
Dátum:	2005
Megjegyzések:	The heart very often becomes a victim of endocrine abnormalities such as thyroid hormone imbalance and insulindeficiency, which are manifested in a broad spectrum of cardiac dysfunction from mildly compromised function tosevere heart failure. These functional changes in the heart are largely independent of alterations in the coronary arteries and instead reside at the level of cardiomyocytes. The status of cardiac function reflects the net of underlying subcellular modifications induced by an increase or decrease in thyroid hormone and insulin plasma levels. Changes in the contractile and regulatory proteins constitute molecular and structural alterations in myofibrillar assembly, called myofibrillar remodeling.These alterations may be adaptive or maladaptive with respect to the functional and metabolic demands on the heart as a consequence of the altered endocrine status in the body. There is a substantial body of information to indicate alterations in myofibrillar proteins including actin, myosin, tropomyosin, troponin, titin, desmin, and myosin-binding protein C in conditions such as hyperthyroidism, hypothyroidism, and diabetes. The present article is focussed on discussion how myofibrillar proteins are altered in response to thyroid hormone imbalance and lack of insulin or its responsiveness, and how their structural and functional changes explain the contractile defects in the heart.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban hyperthyroidism diabetic cardiomyopathy insulin deficiency insulin resistance myofibrillar remodeling
Megjelenés:	Canadian Journal of Physiology and Pharmacology 83 : 12 (2005), p. 1071-1091. -
További szerzők:	Barta Judit (1975-) (kardiológus) Dhalla, Naranjan S.
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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