Mechanisms of Remodelling - A Question of Life (Stem Cell Production) and Death (Myocyte Apoptosis) -

被引:36
作者
Ferrari, Roberto [1 ,2 ]
Ceconi, Claudio [1 ]
Campo, Gianluca [1 ]
Cangiano, Elisa [1 ]
Cavazza, Caterina [1 ]
Secchiero, Paola [3 ]
Tavazzi, Luigi [4 ]
机构
[1] Univ Hosp Ferrara, Chair Cardiol, I-44100 Ferrara, Italy
[2] IRCCS, Fdn Salvatore Maugeri, Ferrara, Italy
[3] Univ Hosp Ferrara, Sez Anat Umana, I-44100 Ferrara, Italy
[4] GVM Hosp Care & Res, Cotignola, Ravenna, Italy
关键词
Apoptosis; Remodeling; Stem cells; ACUTE MYOCARDIAL-INFARCTION; LEFT-VENTRICULAR DYSFUNCTION; CONVERTING ENZYME-INHIBITORS; SEVERE HEART-FAILURE; ANGIOTENSIN-II; CARDIAC MYOCYTES; BONE-MARROW; INDUCED HYPERTROPHY; SURVIVAL; CARVEDILOL;
D O I
10.1253/circj.CJ-09-0573
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Remodeling myocytes show a typical switch between the embryonic and classical features of apoptosis and/or hypertrophy representing a single of death (ie. apoptosis) and it signal of life (ie, hypertrophy). The adult myocyte, however, is a terminal cell; usually it is unable to reproduce and death is not genetically programmed (apoptosis), but occurs by necrosis. The reinstatement of apoptosis and development of hypertrophy during remodeling could be part of the switch forward to the embryonic phenotype with reinstatement of the early embryonic genetic program. Hypertrophy and apoptosis are "sons" of the same "mother": the local. tissue neuroendocrine-neurohumoral response to a mechanical stretch of the myocytes consequent to the geometric changes imposed on the viable myocytes by the necrotic ones. As expected. the life and death cycle is very closely regulated by several autocrine systems. one of which is linked to the interleukin-6 family via a regulatory protein named GP-130. Activation of the GP-130 slows down the death signals. thus favoring hypertrophy and reducing fibrosis (Circ J 2009: 73: 1973-1982)
引用
收藏
页码:1973 / 1982
页数:10
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