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PPARγ in Ischemia-Reperfusion Injury: Overview of the Biology and Therapy.

作者信息

Huang Ruizhen, Zhang Chiyu, Wang Xing, Hu Honglin

机构信息

Department of Urology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.

出版信息

Front Pharmacol. 2021 Apr 28;12:600618. doi: 10.3389/fphar.2021.600618. eCollection 2021.


DOI:10.3389/fphar.2021.600618
PMID:33995008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8117354/
Abstract

Ischemia-reperfusion injury (IRI) is a complex pathophysiological process that is often characterized as a blood circulation disorder caused due to various factors (such as traumatic shock, surgery, organ transplantation, burn, and thrombus). Severe metabolic dysregulation and tissue structure destruction are observed upon restoration of blood flow to the ischemic tissue. Theoretically, IRI can occur in various tissues and organs, including the kidney, liver, myocardium, and brain, among others. The advances made in research regarding restoring tissue perfusion in ischemic areas have been inadequate with regard to decreasing the mortality and infarct size associated with IRI. Hence, the clinical treatment of patients with severe IRI remains a thorny issue. Peroxisome proliferator-activated receptor (PPARγ) is a member of a superfamily of nuclear transcription factors activated by agonists and is a promising therapeutic target for ameliorating IRI. Therefore, this review focuses on the role of PPARγ in IRI. The protective effects of PPARγ, such as attenuating oxidative stress, inhibiting inflammatory responses, and antagonizing apoptosis, are described, envisaging certain therapeutic perspectives.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62fb/8117354/e6c29f758ebb/fphar-12-600618-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62fb/8117354/e6c29f758ebb/fphar-12-600618-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62fb/8117354/e6c29f758ebb/fphar-12-600618-g001.jpg

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[2]
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[3]
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Int J Med Sci. 2025-1-1

[4]
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J Clin Transl Hepatol. 2023-12-28

[5]
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[6]
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Pharmaceuticals (Basel). 2022-12-21

[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Cilostazol mitigates mesenteric ischemia/reperfusion-induced lung lesion: Contribution of PPAR-γ, NF-κB, and STAT3 crosstalk.

Life Sci. 2021-2-1

[2]
Chrysin rescues rat myocardium from ischemia-reperfusion injury via PPAR-γ/Nrf2 activation.

Eur J Pharmacol. 2020-9-15

[3]
Cafestol preconditioning attenuates apoptosis and autophagy during hepatic ischemia-reperfusion injury by inhibiting ERK/PPARγ pathway.

Int Immunopharmacol. 2020-7

[4]
-Sitosterol Protects against Myocardial Ischemia/Reperfusion Injury via Targeting PPAR/NF-B Signalling.

Evid Based Complement Alternat Med. 2020-3-28

[5]
Dexmedetomidine preconditioning alleviated murine liver ischemia and reperfusion injury by promoting macrophage M2 activation via PPARγ/STAT3 signaling.

Int Immunopharmacol. 2020-3-4

[6]
Pioglitazone Attenuates Reoxygenation Injury in Renal Tubular NRK-52E Cells Exposed to High Glucose Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress.

Front Pharmacol. 2020-1-23

[7]
PPARγ-Independent Side Effects of Thiazolidinediones on Mitochondrial Redox State in Rat Isolated Hearts.

Cells. 2020-1-20

[8]
Sevoflurane Protects against Intestinal Ischemia-Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma/Nuclear Factor-κB Pathway in Rats.

Pharmacology. 2019-10-25

[9]
Pioglitazone protects tubular cells against hypoxia/reoxygenation injury through enhancing autophagy via AMPK-mTOR signaling pathway.

Eur J Pharmacol. 2019-9-24

[10]
Suppression of microRNA‑27a protects against liver ischemia/reperfusion injury by targeting PPARγ and inhibiting endoplasmic reticulum stress.

Mol Med Rep. 2019-9-3

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