Caloric restriction mimetics for the treatment of cardiovascular diseases

被引:31
作者
Sciarretta, Sebastiano [1 ,2 ]
Forte, Maurizio [2 ]
Castoldi, Francesca [3 ,4 ]
Frati, Giacomo [1 ,2 ]
Versaci, Francesco [5 ]
Sadoshima, Junichi [6 ]
Kroemer, Guido [3 ,4 ,7 ,8 ,9 ]
Maiuri, Maria Chiara [3 ,4 ]
机构
[1] Sapienza Univ Rome, Dept Med Surg Sci & Biotechnol, Corso Repubbl 79, I-40100 Latina, Italy
[2] IRCCS Neuromed, Dept AngioCardioNeurol, Pozzilli, IS, Italy
[3] Sorbonne Univ, Team Metab Canc & Immun, Ctr Rech Cordeliers, INSERM UMRS1138,Univ Paris, F-75006 Paris, France
[4] Gustave Roussy Canc Campus, Cell Biol & Metabol Platforms, F-94805 Villejuif, France
[5] S Maria Goretti Hosp, Div Cardiol, I-04100 Latina, Italy
[6] Rutgers New Jersey Med Sch, Dept Cell Biol & Mol Med, 185 South Orange Ave,G-609, Newark, NJ 07103 USA
[7] Hop Europeen Georges Pompidou, AP HP, Pole Biol, F-75015 Paris, France
[8] Chinese Acad Sci, Suzhou Inst Syst Med, Suzhou 215163, Jiangsu, Peoples R China
[9] Karolinska Univ Hosp, Karolinska Inst, Dept Womens & Childrens Hlth, S-17176 Stockholm, Sweden
基金
欧盟地平线“2020”;
关键词
Caloric restriction mimetics; Cardiovascular diseases; Autophagy; Cardiac ageing; Starvation; ISCHEMIA-REPERFUSION INJURY; ATTENUATES CARDIAC-HYPERTROPHY; ATP CITRATE-LYASE; LIFE-SPAN; OXIDATIVE-STRESS; EPIGALLOCATECHIN GALLATE; GREEN TEA; CARDIOMYOCYTE APOPTOSIS; HEART-FAILURE; ISCHEMIA/REPERFUSION INJURY;
D O I
10.1093/cvr/cvaa297
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Caloric restriction mimetics (CRMs) are emerging as potential therapeutic agents for the treatment of cardiovascular diseases. CRMs include natural and synthetic compounds able to inhibit protein acetyltransferases, to interfere with acetyl coenzyme A biosynthesis, or to activate (de)acetyltransferase proteins. These modifications mimic the effects of caloric restriction, which is associated with the activation of autophagy. Previous evidence demonstrated the ability of CRMs to ameliorate cardiac function and reduce cardiac hypertrophy and maladaptive remodelling in animal models of ageing, mechanical overload, chronic myocardial ischaemia, and in genetic and metabolic cardiomyopathies. In addition, CRMs were found to reduce acute ischaemia-reperfusion injury. In many cases, these beneficial effects of CRMs appeared to be mediated by autophagy activation. In the present review, we discuss the relevant literature about the role of different CRMs in animal models of cardiac diseases, emphasizing the molecular mechanisms underlying the beneficial effects of these compounds and their potential future clinical application.
引用
收藏
页码:1434 / 1449
页数:16
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