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001-es BibID:	BIBFORM015749
Első szerző:	Barta Judit (kardiológus)
Cím:	Myofibrillar Remodeling During the Development of Ischemic Heart Disease / Barta Judit, Raja B. Singh, Srilekha Maddika, Rajat Sethi, Naranjan S. Dhalla
Dátum:	2008
Megjegyzések:	Ischemic heart disease (IHD) resulting from insufficient supply of O2 and nutrients is one of the major causes of moitality and morbidity in the developed as well as developing countries. Extensive studies on IHD haverevealed alterations at the cellular, subcellular and molecular levels in the ischemic cardiac muscle. It is generally believed that both the occurrences of oxidativestress and the development of intracellular calcium (Ca2+) overload are important mechanisms of cardiac dysfunction and injury to myocardium in the IHD. Myofibrílar proteins, which form an essential part of contractile machinery ofthe heart and determine the cardiac contractile activity have been shown to exhibit changes in their assembly as well as activities under a wide variety of conditions associated with IHD. The present article is aimed to provide an insight into the assembly of myofibrilar proteins and alterations in their biochemical activities to emphasize the significance of myofibrillar remodeling(changes in structure and function) in hearts subjected to ischemia as well as reperfusion. It is proposed that myofibrillar remodeling plays an important role in cardiac dysftrnction in IHD.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok könyvfejezet Ischemic heart disease myofibrillar remodeling ischemia-reperfusion injury
Megjelenés:	Recent Advances in Cardiovascular Sciences / ed. S.S. Agrawal. - p. 42-62
További szerzők:	Singh, Raja B. Maddika, Srilekha Sethi, Rajat Dhalla, Naranjan S.
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM015747
Első szerző:	Dhalla, Naranjan S.
Cím:	Subcellular Remodeling as a Viable Target for the Treatment of Congestive Heart Failure / Naranjan S. Dhalla, Melissa R. Dent, Paramjit S. Tappia, Rajat Sethi, Barta Judit, Ramesh K. Goyal
Dátum:	2006
Megjegyzések:	It is now well known that congestive heart failure (CHF) is invariably associated with cardiac hypertrophy, and changes in the shape and size of cardiomyocytes (cardiac remodeling) are considered to explain cardiac dysfunction in CHF. However, the mechanisms responsible for the transition of cardiac hypertrophy to heart failure are poorly understood. Several lines of evidence both from various experimental models of CHF and from patients with different types of CHF have indicated that the functions of different subcellular organelles such as extracellular matrix, sarcolemma, sarcoplasmic reticulum, myofibrils, mitochondria, and nucleus are defective. Subcellular abnormalities for protein contents, gene expression, andenzyme activities in the failing heart become evident as a consequence of prolonged hormonal imbalance, metabolic derangements, and cation maldistribution. In particular, the occurrence of oxidative stress, development of intracellular Ca2+ overload, activation of proteasesand phospholipases, and alterations in cardiac gene expression result in changes in the biochemical composition, molecular structure, and function of different subcellular organelles (subcellular remodeling). Not only does subcellular remodeling appear to be intimately involved in the transition of cardiac hypertrophy to heart failure, the mismatching of the function of different subcellular organelles leads to the development of cardiac dysfunction. Although blockade of the renin-angiotensin system, sympathetic nervous system, and various other hormonal actions have been reported to produce beneficial effects on cardiac remodeling and heart dysfunction in CHF, the actions of various cardiac drugs on subcellular remodeling have not been examined extensively. Some recent studies have indicated thatboth the angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists attenuate changes in sarcolemma, sarcoplasmic reticulum, and myofibril enzyme activities, protein contents, and gene expression, and partly improve cardiac function in the failing hearts. It is suggested that subcellular remodeling is an excellent target for the development of improved drug therapy for CHF. Furthermore, extensive studies should investigate theeffects of different agents individually or in combination on reverse subcellular remodeling, cardiac remodeling, and cardiac dysfunction in various experimental models of CHF.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban congestive heart failure cardiac remodeling subcellular remodeling cardiac drugs cardiac hypertrophy cardiac dysfunction
Megjelenés:	Journal of Cardiovascular Pharmacology and Therapeutics. - 11 : 1 (2006), p. 31-45. -
További szerzők:	Dent, Melissa R. Tappia, Paramjit S. Sethi, Rajat Barta Judit (1975-) (kardiológus) Goyal, Ramesh K.
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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