Journalartikel
Autorenliste: Rohrbach, Susanne; Aslam, Muhammad; Niemann, Bernd; Schulz, Rainer
Jahr der Veröffentlichung: 2014
Seiten: 2964-2992
Zeitschrift: British Journal of Pharmacology
Bandnummer: 171
Heftnummer: 12
ISSN: 0007-1188
eISSN: 1476-5381
Open Access Status: Green
DOI Link: https://doi.org/10.1111/bph.12650
Verlag: Wiley
Abstract:
Caloric restriction (CR) is the most reliable intervention to extend lifespan and prevent age-related disorders in various species from yeast to rodents. Short- and long-term CR confers cardio protection against ischaemia/reperfusion injury in young and even in aged rodents. A few human trials suggest that CR has the potential to mediate improvement of cardiac or vascular function and induce retardation of cardiac senescence also in humans. The underlying mechanisms are diverse and have not yet been clearly defined. Among the known mediators for the benefits of CR are NO, the AMP-activated PK, sirtuins and adiponectin. Mitochondria, which play a central role in such complex processes within the cell as apoptosis, ATP-production or oxidative stress, are centrally involved in many aspects of CR-induced protection against ischaemic injury. Here, we discuss the relevant literature regarding the protection against myocardial ischaemia/reperfusion injury conferred by CR. Furthermore, we will discuss drug targets to mimic CR and the possible role of calorie restriction in preserving cardiovascular function in humans.
Zitierstile
Harvard-Zitierstil: Rohrbach, S., Aslam, M., Niemann, B. and Schulz, R. (2014) Impact of caloric restriction on myocardial ischaemia/reperfusion injury and new therapeutic options to mimic its effects, British Journal of Pharmacology, 171(12), pp. 2964-2992. https://doi.org/10.1111/bph.12650
APA-Zitierstil: Rohrbach, S., Aslam, M., Niemann, B., & Schulz, R. (2014). Impact of caloric restriction on myocardial ischaemia/reperfusion injury and new therapeutic options to mimic its effects. British Journal of Pharmacology. 171(12), 2964-2992. https://doi.org/10.1111/bph.12650
Schlagwörter
AMPK; CARDIOVASCULAR RISK-FACTORS; COMPLEX-I ACTIVITY; CR mimetic; FATTY-ACID OXIDATION; INDUCED CARDIAC-HYPERTROPHY; ISCHEMIA-REPERFUSION INJURY; LEFT-VENTRICULAR HYPERTROPHY; LOW-FLOW ISCHEMIA; mitobiogenesis; sirtuin; SMALL-MOLECULE ACTIVATORS