PMID- 35336822
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220329
IS  - 2079-7737 (Print)
IS  - 2079-7737 (Electronic)
IS  - 2079-7737 (Linking)
VI  - 11
IP  - 3
DP  - 2022 Mar 16
TI  - AMPK Activation Is Indispensable for the Protective Effects of Caloric 
      Restriction on Left Ventricular Function in Postinfarct Myocardium.
LID - 10.3390/biology11030448 [doi]
LID - 448
AB  - BACKGROUND: Caloric restriction (CR) extends lifespan in many species, including 
      mammals. CR is cardioprotective in senescent myocardium by correcting 
      pre-existing mitochondrial dysfunction and apoptotic activation. Furthermore, it 
      confers cardioprotection against acute ischemia-reperfusion injury. Here, we 
      investigated the role of AMP-activated protein kinase (AMPK) in mediating the 
      cardioprotective CR effects in failing, postinfarct myocardium. METHODS: Ligation 
      of the left coronary artery or sham operation was performed in rats and mice. 
      Four weeks after surgery, left ventricular (LV) function was analyzed by 
      echocardiography, and animals were assigned to different feeding groups (control 
      diet or 40% CR, 8 weeks) as matched pairs. The role of AMPK was investigated with 
      an AMPK inhibitor in rats or the use of alpha 2 AMPK knock-out mice. RESULTS: CR 
      resulted in a significant improvement in LV function, compared to postinfarct 
      animals receiving control diet in both species. The improvement in LV function 
      was accompanied by a reduction in serum BNP, decrease in LV proapoptotic 
      activation, and increase in mitochondrial biogenesis in the LV. Inhibition or 
      loss of AMPK prevented most of these changes. CONCLUSIONS: The failing, 
      postischemic heart is protected from progressive loss of LV systolic function by 
      CR. AMPK activation is indispensable for these protective effects.
FAU - Niemann, Bernd
AU  - Niemann B
AD  - Department of Cardiac and Vascular Surgery, University Hospital Giessen and 
      Marburg, Justus Liebig University Giessen, 35392 Giessen, Germany.
AD  - Department of Cardiothoracic Surgery, Martin Luther University Halle-Wittenberg, 
      06097 Halle, Germany.
FAU - Pan, Ruping
AU  - Pan R
AD  - Institute of Physiology, Justus Liebig University Giessen, 35392 Giessen, 
      Germany.
FAU - Issa, Hassan
AU  - Issa H
AD  - Klinik fur Kinder und Jugendliche, Evangelisches Krankenhaus Oberhausen, 46047 
      Oberhausen, Germany.
FAU - Simm, Andreas
AU  - Simm A
AD  - Department of Cardiothoracic Surgery, Martin Luther University Halle-Wittenberg, 
      06097 Halle, Germany.
FAU - Schulz, Rainer
AU  - Schulz R
AUID- ORCID: 0000-0003-3017-0476
AD  - Institute of Physiology, Justus Liebig University Giessen, 35392 Giessen, 
      Germany.
FAU - Rohrbach, Susanne
AU  - Rohrbach S
AUID- ORCID: 0000-0002-7523-5221
AD  - Institute of Physiology, Justus Liebig University Giessen, 35392 Giessen, 
      Germany.
LA  - eng
GR  - 268555672 - SFB 1213, Project B03/Deutsche Forschungsgemeinschaft/
GR  - Rusche Grant/Deutsche Herzstiftung/
PT  - Journal Article
DEP - 20220316
PL  - Switzerland
TA  - Biology (Basel)
JT  - Biology
JID - 101587988
PMC - PMC8945456
OTO - NOTNLM
OT  - AMPK
OT  - caloric restriction
OT  - heart failure
OT  - ischemia
OT  - mitochondria
COIS- The authors declare no conflict of interest.
EDAT- 2022/03/27 06:00
MHDA- 2022/03/27 06:01
PMCR- 2022/03/16
CRDT- 2022/03/26 01:07
PHST- 2022/01/30 00:00 [received]
PHST- 2022/03/02 00:00 [revised]
PHST- 2022/03/08 00:00 [accepted]
PHST- 2022/03/26 01:07 [entrez]
PHST- 2022/03/27 06:00 [pubmed]
PHST- 2022/03/27 06:01 [medline]
PHST- 2022/03/16 00:00 [pmc-release]
AID - biology11030448 [pii]
AID - biology-11-00448 [pii]
AID - 10.3390/biology11030448 [doi]
PST - epublish
SO  - Biology (Basel). 2022 Mar 16;11(3):448. doi: 10.3390/biology11030448.