PMID- 24278863
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20131126
LR  - 20211021
IS  - 2288-176X (Print)
IS  - 2288-1778 (Electronic)
IS  - 2288-176X (Linking)
VI  - 9
IP  - 2
DP  - 2013 Apr
TI  - Effects of aging and exercise training on apoptosis in the heart.
PG  - 212-9
LID - 10.12965/jer.130002 [doi]
AB  - Aging is characterized by a progressive decline in cardiac function. A critical 
      contributor to the age-related impairment in cardiac function is the loss of 
      cardiac myocytes through "apoptosis", or programmed cell death. Structural 
      remodeling in the heart with advancing age includes (a) loss of cardiomyocytes, 
      (b) reactive hypertrophy of the remaining cardiomyocytes, and (c) increased 
      connective tissue and altered geometry. The loss of cardiomyocytes with aging 
      occurs through apoptosis. Particularly, mitochondrial-mediated apoptotic pathway 
      is the best characterized and believed critical in regulating apoptosis with 
      aging, suggesting that mitochondria are very important sites of programmed cell 
      death. It has been also reported that mitochondrial dysfunction, oxidative 
      stress, and impaired stress response contribute to age-induced mechanical 
      remodeling as well as apoptosis. In contrast, exercise training not only improves 
      cardiac function, but also reduces the risk of heart disease. We recently found 
      that aging increased mitochondrial-mediated apoptotic signaling and apoptosis in 
      the left ventricle, while chronic exercise training was effective in diminishing 
      mitochondrial-mediated apoptotic signaling pathways in the aging heart, as 
      indicated by lower DNA fragmentation, terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL)-positive staining, and 
      caspase-3 cleavage, when compared with left ventricles from the age-matched 
      sedentary group. In this review, we will provide a comprehensive update regarding 
      the effects of aging and exercise training on apoptosis in the heart.
FAU - Kwak, Hyo-Bum
AU  - Kwak HB
AD  - Department of Kinesiology, Inha University, Incheon, Korea.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20130425
PL  - Korea (South)
TA  - J Exerc Rehabil
JT  - Journal of exercise rehabilitation
JID - 101615171
EIN - J Exerc Rehabil. 2013 Dec;9(6):549
PMC - PMC3836520
OTO - NOTNLM
OT  - Aging
OT  - Apoptosis
OT  - Heart
OT  - Mitochondria
OT  - Myocytes
EDAT- 2013/11/28 06:00
MHDA- 2013/11/28 06:01
PMCR- 2013/04/25
CRDT- 2013/11/27 06:00
PHST- 2013/02/03 00:00 [received]
PHST- 2013/03/04 00:00 [revised]
PHST- 2013/04/02 00:00 [accepted]
PHST- 2013/11/27 06:00 [entrez]
PHST- 2013/11/28 06:00 [pubmed]
PHST- 2013/11/28 06:01 [medline]
PHST- 2013/04/25 00:00 [pmc-release]
AID - jer-9-2-2-212_219 [pii]
AID - 10.12965/jer.130002 [doi]
PST - ppublish
SO  - J Exerc Rehabil. 2013 Apr;9(2):212-9. doi: 10.12965/jer.130002. Epub 2013 Apr 25.