000102182 001__ 102182
000102182 005__ 20230519145442.0
000102182 0247_ $$2doi$$a10.1155/2021/8876792
000102182 0248_ $$2sideral$$a124147
000102182 037__ $$aART-2021-124147
000102182 041__ $$aeng
000102182 100__ $$aSegovia-Roldan, M.
000102182 245__ $$aMelatonin to rescue the aged heart: antiarrhythmic and antioxidant benefits
000102182 260__ $$c2021
000102182 5060_ $$aAccess copy available to the general public$$fUnrestricted
000102182 5203_ $$aAging comes with gradual loss of functions that increase the vulnerability to disease, senescence, and death. The mechanisms underlying these processes are linked to a prolonged imbalance between damage and repair. Damaging mechanisms include oxidative stress, mitochondrial dysfunction, chronodisruption, inflammation, and telomere attrition, as well as genetic and epigenetic alterations. Several endogenous tissue repairing mechanisms also decrease. These alterations associated with aging affect the entire organism. The most devastating manifestations involve the cardiovascular system and may lead to lethal cardiac arrhythmias. Together with structural remodeling, electrophysiological and intercellular communication alterations during aging predispose to arrhythmic events. Despite the knowledge on repairing mechanisms in the cardiovascular system, effective antiaging strategies able to reduce the risk of arrhythmias are still missing. Melatonin is a promising therapeutic candidate due to its pleiotropic actions. This indoleamine regulates chronobiology and endocrine physiology. Of relevance, melatonin is an antiaging, antioxidant, antiapoptotic, antiarrhythmic, immunomodulatory, and antiproliferative molecule. This review focuses on the protective effects of melatonin on age-induced cardiac functional and structural alterations, potentially becoming a new fountain of youth for the heart.
000102182 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000102182 590__ $$a7.31$$b2021
000102182 592__ $$a1.233$$b2021
000102182 594__ $$a9.3$$b2021
000102182 591__ $$aCELL BIOLOGY$$b55 / 195 = 0.282$$c2021$$dQ2$$eT1
000102182 593__ $$aBiochemistry$$c2021$$dQ1
000102182 593__ $$aMedicine (miscellaneous)$$c2021$$dQ1
000102182 593__ $$aCell Biology$$c2021$$dQ1
000102182 655_4 $$ainfo:eu-repo/semantics/review$$vinfo:eu-repo/semantics/publishedVersion
000102182 700__ $$aDiez, E.R.
000102182 700__ $$0(orcid)0000-0002-1960-407X$$aPueyo, E.$$uUniversidad de Zaragoza
000102182 7102_ $$15008$$2800$$aUniversidad de Zaragoza$$bDpto. Ingeniería Electrón.Com.$$cÁrea Teoría Señal y Comunicac.
000102182 773__ $$g2021, 8876792 (2021), [18 pp.]$$pOxidative Medicine and Cellular Longevity$$tOxidative Medicine and Cellular Longevity$$x1942-0900
000102182 8564_ $$s1115254$$uhttps://zaguan.unizar.es/record/102182/files/texto_completo.pdf$$yVersión publicada
000102182 8564_ $$s2483448$$uhttps://zaguan.unizar.es/record/102182/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000102182 909CO $$ooai:zaguan.unizar.es:102182$$particulos$$pdriver
000102182 951__ $$a2023-05-18-14:34:39
000102182 980__ $$aARTICLE