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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2019.1
- 수록면
- 292 - 300 (9page)
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Immunometabolism, defined as the interaction of metabolic pathways with the immune system, influences the pathogenesis of metabolic diseases. Metformin and carbon monoxide (CO) are two pharmacological agents known to ameliorate metabolic disorders. There are notable similarities and differences in the reported effects of metformin and CO on immunometabolism. Metformin, an anti-diabetes drug, has positive effects on metabolism and can exert antiinflammatory and anti-cancer effects via adenosine monophosphate-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms. CO, an endogenous product of heme oxygenase-1 (HO-1), can exert anti-inflammatory and antioxidant effects at low concentration. CO can confer cytoprotection in metabolic disorders and cancer via selective activation of the protein kinase R-like endoplasmic reticulum (ER) kinase (PERK) pathway. Both metformin and CO can induce mitochondrial stress to produce a mild elevation of mitochondrial ROS (mtROS) by distinct mechanisms. Metformin inhibits complex I of the mitochondrial electron transport chain (ETC), while CO inhibits ETC complex IV. Both metformin and CO can differentially induce several protein factors, including fibroblast growth factor 21 (FGF21) and sestrin2 (SESN2), which maintain metabolic homeostasis; nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of the antioxidant response; and REDD1, which exhibits an anticancer effect. However, metformin and CO regulate these effects via different pathways. Metformin stimulates p53- and AMPK-dependent pathways whereas CO can selectively trigger the PERK-dependent signaling pathway. Although further studies are needed to identify the mechanistic differences between metformin and CO, pharmacological application of these agents may represent useful strategies to ameliorate metabolic diseases associated with altered immunometabolism.
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참고문헌 (85)
참고문헌 신청
Alberti, K. G. / 2009 / Harmonizing the metabolic syndrome : a joint interim statement of the international diabetes federation task force on epidemiology and prevention; national heart, lung, and blood institute; american heart association; world heart federation;international atherosclerosis society; and international association for the study of obesity / Circulation 120:1640~1645
Ashabi, G. / 2015 / Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia / Metab. Brain Dis 30:747~754
Ben Sahra, I. / 2011 / Metformin, independent of AMPK, induces mTOR inhibition and cell-cycle arrest through REDD1 / Cancer Res 71:4366~4372
Boucher, J. / 2014 / Insulin receptor signaling in normal and insulin-resistant states. Cold Spring Harb Perspect. Biol / Cold Spring Harb Perspect. Biol 6
Bray, G. A. / 2004 / Medical consequences of obesity / J. Clin. Endocrinol. Metab 89:2583~2589
Ashabi, G. / 2015 / Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia / Metab. Brain Dis 30:747~754
Ben Sahra, I. / 2011 / Metformin, independent of AMPK, induces mTOR inhibition and cell-cycle arrest through REDD1 / Cancer Res 71:4366~4372
Boucher, J. / 2014 / Insulin receptor signaling in normal and insulin-resistant states. Cold Spring Harb Perspect. Biol / Cold Spring Harb Perspect. Biol 6
Bray, G. A. / 2004 / Medical consequences of obesity / J. Clin. Endocrinol. Metab 89:2583~2589
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