Találati lista | Tudóstér

001-es BibID:	BIBFORM067699
Első szerző:	Lekli István (gyógyszerész)
Cím:	Autophagy : an adaptive physiologic countermeasure to cellular senescence and ischemia/reperfusion-associated cardiac arrhythmias / Lekli István, David Donald Haines, Balla György, Tósaki Árpád
Dátum:	2017
ISSN:	1582-1838
Megjegyzések:	Oxidative stress placed on tissues involved in pathogenesis of a disease, activates compensatory metabolic changes, such as DNA damage repair that in turn, cause intracellular accumulation of detritus and "proteotoxic stress", leading to emergence of "senescent" cellular phenotypes, which express high levels of inflammatory mediators, resulting in degradation of tissue function. Proteotoxic stress resulting from hyperactive inflammation following reperfusion of ischemic tissue, causes accumulation of proteinaceous debris in cells of the heart in ways that cause potentially fatal arrhythmias, in particular, ventricular fibrillation (VF). An adaptive response to VF is occurrence of autophagy, an intracellular bulk degradation of damaged macromolecules and organelles that may restore cellular and tissue homeostasis, improving chances for recovery. Nevertheless, depending on the type and intensity of stressors and inflammatory responses, autophagy may become pathological, resulting in excessive cell death. The present review examines the multilayered defenses cells have evolved to reduce proteotoxic stress by degradation of potentially toxic material beginning with endoplasmic reticulum-associated degradation; and the unfolded protein response, which are mechanisms for removal from the ER of misfolded proteins; then progressing through the stages of autophagy, including descriptions of autophagosomes and related vesicular structures which process material for degradation and autophagy-associated proteins including Beclin-1 and regulatory complexes. The physiologic roles of each mode of proteotoxic defense will be examined along with consideration of how emerging understanding of autophagy, along with a newly discovered regulatory cell type called telocytes, may be used to augment existing strategies for prevention and management of cardiovascular disease.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban Autophagy cardiovascular system proteotoxic stress
Megjelenés:	Journal of Cellular and Molecular Medicine. - 21 : 6 (2017), p. 1058-1072. -
További szerzők:	Haines, David Donald (1981-) (gyógyszerész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:	OTKA-104017 OTKA OTKA-111794 OTKA TÁMOP-4.2.4.A/2-11-1-2012-0001 TÁMOP GINOP-2.3.2-15 GINOP EFOP-3.6.1 EFOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: