TY - JOUR
T1 - Serum Glucocorticoid-Regulated Kinase-1 in Ischemia-Reperfusion Injury
T2 - Blessing or Curse
AU - Mozaffari, Mahmood S.
N1 - Publisher Copyright:
Copyright © 2023 by The American Society for Pharmacology and Experimental Therapeutics.
PY - 2023/12/1
Y1 - 2023/12/1
N2 - The family of serum-glucocorticoid-regulated kinase (SGK) consists of three paralogs, SGK-1, SGK-2, and SGK-3, with SGK-1 being the better studied. Indeed, recognition of the role of SGK-1 in regulation of cell survival and proliferation has led to introduction of a number of small-molecule inhibitors for some types of cancer. In addition, SGK-1 regulates major physiologic effects, such as renal solute transport, and contributes to the pathogenesis of non-neoplastic conditions involving major organs including the heart and the kidney. These observations raise the prospect for therapeutic modulation of SGK-1 to reduce the burden of such diseases as myocardial infarction and acute kidney injury. Following a brief description of the structure and function of SGK family of proteins, the present review is primarily focused on our current understanding of the role of SGK-1 in pathologies related to ischemia-reperfusion injury involving several organs (e.g., heart, kidney). The essential role of the mitochondrial permeability transition pore in cell death coupled with the pro-survival function of SGK-1 raise the prospect that its therapeutic modulation could beneficially impact conditions associated with ischemia-reperfusion injury.
AB - The family of serum-glucocorticoid-regulated kinase (SGK) consists of three paralogs, SGK-1, SGK-2, and SGK-3, with SGK-1 being the better studied. Indeed, recognition of the role of SGK-1 in regulation of cell survival and proliferation has led to introduction of a number of small-molecule inhibitors for some types of cancer. In addition, SGK-1 regulates major physiologic effects, such as renal solute transport, and contributes to the pathogenesis of non-neoplastic conditions involving major organs including the heart and the kidney. These observations raise the prospect for therapeutic modulation of SGK-1 to reduce the burden of such diseases as myocardial infarction and acute kidney injury. Following a brief description of the structure and function of SGK family of proteins, the present review is primarily focused on our current understanding of the role of SGK-1 in pathologies related to ischemia-reperfusion injury involving several organs (e.g., heart, kidney). The essential role of the mitochondrial permeability transition pore in cell death coupled with the pro-survival function of SGK-1 raise the prospect that its therapeutic modulation could beneficially impact conditions associated with ischemia-reperfusion injury.
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U2 - 10.1124/jpet.123.001846
DO - 10.1124/jpet.123.001846
M3 - Article
C2 - 37770199
AN - SCOPUS:85179070900
SN - 0022-3565
VL - 387
SP - 277
EP - 287
JO - Journal of Pharmacology and Experimental Therapeutics
JF - Journal of Pharmacology and Experimental Therapeutics
IS - 3
ER -