PMID- 12022752
OWN - NLM
STAT- MEDLINE
DCOM- 20021129
LR  - 20190916
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 17
IP  - 5
DP  - 2002 May
TI  - The interaction between Hsp70 and TNF-alpha expression: a novel mechanism for 
      protection of the myocardium against post-injury depression.
PG  - 345-53
AB  - Tumor necrosis factor-alpha (TNF-alpha) depresses myocardial contractility, and 
      overexpression of TNF-alpha in the myocardium contributes to cardiac dysfunction 
      caused by both systemic and local insults. Sepsis, endotoxemia, hemorrhagic 
      shock, and myocardial ischemia-reperfusion all promote cardiac dysfunction in 
      part by a TNF-alpha-mediated mechanism. Thus, TNF-alpha represents an appealing 
      therapeutic target for myocardial protection against multiple clinically relevant 
      insults. The inducible 70-kD heat shock protein (Hsp70) is expressed in the 
      myocardium in response to stress and has been linked to enhanced myocardial 
      resistance to depression associated with ischemia-reperfusion or sepsis. The 
      mechanism by which Hsp70 protects cardiac function against a subsequent insult 
      remains obscure. In vitro induction of Hsp70 in monocytes or macrophages inhibits 
      TNF-alpha production following bacterial lipopolysaccharide stimulation, and in 
      vivo induction of Hsp70 down-regulates tissue TNF-alpha production following an 
      injurious insult. Understanding of the regulatory role of Hsp70 in the myocardial 
      inflammatory response will provide insights into the mechanism by which Hsp70 
      preserves cardiac function and may yield therapies for protection of the 
      myocardium against depression associated injurious insults.
FAU - Meng, Xianzhong
AU  - Meng X
AD  - Department of Surgery, University of Colorado Health Sciences Center, Denver, 
      USA.
FAU - Harken, Alden H
AU  - Harken AH
LA  - eng
GR  - GM-08315/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (HSP70 Heat-Shock Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Endotoxemia/complications/metabolism/physiopathology
MH  - HSP70 Heat-Shock Proteins/*physiology
MH  - Heart/*physiology
MH  - Heart Diseases/*etiology/therapy
MH  - Humans
MH  - Myocardial Ischemia/complications/metabolism/physiopathology
MH  - Myocardial Reperfusion Injury/complications/metabolism/physiopathology
MH  - NF-kappa B/metabolism
MH  - Sepsis/complications/metabolism/physiopathology
MH  - Shock, Hemorrhagic/complications/metabolism/physiopathology
MH  - Tumor Necrosis Factor-alpha/*physiology
RF  - 137
EDAT- 2002/05/23 10:00
MHDA- 2002/11/30 04:00
CRDT- 2002/05/23 10:00
PHST- 2002/05/23 10:00 [pubmed]
PHST- 2002/11/30 04:00 [medline]
PHST- 2002/05/23 10:00 [entrez]
AID - 10.1097/00024382-200205000-00001 [doi]
PST - ppublish
SO  - Shock. 2002 May;17(5):345-53. doi: 10.1097/00024382-200205000-00001.