Department of Urology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Department of Endocrinology, The Fourth Affiliated Hospital of Nanchang University, Nanchang, China.
Oxid Med Cell Longev. 2022 Aug 30;2022:7142314. doi: 10.1155/2022/7142314. eCollection 2022.
Renal ischemia-reperfusion injury (RIRI) is a common pathological process that causes kidney injury. Previous studies have indicated that both peroxisome proliferator-activated receptor (PPAR) and microRNA-21 (miR-21) exert protective effects against RIRI. However, their relationship is not well understood. In the present study, we investigated the role of the PPAR/miR-21/programmed cell death 4 (PDCD4) axis in IRI, both and . cell hypoxia/reoxygenation (H/R) and RIRI models were established, and cell viability, cell apoptosis, and key molecule expression profiles were analyzed. Our results showed that both PPAR and miR-21 had protective effects against RIRI to varying degrees, and there was an interaction between PPAR and miR-21. PPAR could promote the expression of miR-21 and partially protect against RIRI by reducing the level of the miR-21 target protein (PDCD4). Our findings underscore the potential utility of future clinical investigations of PPAR activation and targeting of the underlying miR-21/PDCD4/caspase-3 pathway, which may participate in the pathogenesis of human IRI.
肾缺血再灌注损伤(RIRI)是一种常见的引起肾损伤的病理过程。先前的研究表明,过氧化物酶体增殖物激活受体(PPAR)和 microRNA-21(miR-21)都对 RIRI 具有保护作用。然而,它们之间的关系尚不清楚。在本研究中,我们研究了 PPAR/miR-21/程序性细胞死亡 4(PDCD4)轴在 IRI 中的作用,包括细胞缺氧/复氧(H/R)和体内 RIRI 模型,并分析了细胞活力、细胞凋亡和关键分子表达谱。我们的结果表明,PPAR 和 miR-21 都对 RIRI 具有不同程度的保护作用,并且它们之间存在相互作用。PPAR 可以促进 miR-21 的表达,并通过降低 miR-21 靶蛋白(PDCD4)的水平来部分保护 RIRI。我们的研究结果强调了未来对 PPAR 激活和针对潜在的 miR-21/PDCD4/caspase-3 通路的临床研究的潜在应用价值,该通路可能参与了人类 IRI 的发病机制。