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<p>Chronic kidney disorder is a rising danger to health that affects a significant percentage of older adults, and a crucial stage in its development is fibrosis. MicroRNAs and transforming_ growth factor-β1(TGF-β1) /SMAD2 signal pathway significantly regulate this process. miR-34a promotes extracellular matrix (ECM) deposition and inhibits B cell lymphoma-2 (Bcl-2), a target gene with antifibrotic properties shown to protect against renal fibrosis in animal models. Currently, several drugs, including entacapone, have been reported to suppress miR-34a activation. Experimental model of Carbon- tetrachloride (CCl<sub>4</sub>)-induced renal fibrosis revealed elevated serum levels of urea and creatinine, an increased urinary microalbumin-to-creatinine ratio, deterioration of the antioxidant-oxidant balance, an increase in TGF-β1 in renal tissue, and increased renal miR–34a–SMAD2 expression were observed, accompanied by decreased expression of Bcl-2. Entacapone holds reno-protective promises likely via its anti-inflammatory-antioxidant effects in CCl<sub>4</sub>-induced renal fibrosis by favorable modulation of miR-34a /TGF-β1/SMAD2 Signaling Pathway.</p>

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Entacapone’s therapeutic potential in renal fibrosis by targeting miR-34a/TGFβ1/Smad2 signaling: an experimental rat model study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月12日

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  • Yosra M. Magdy,
  • Sherif A. Kamar,
  • Tamer M. M. Abuamara,
  • Yomna M. Tamim,
  • Hayam Ateyya,
  • Marwa Tarek,
  • Nehal Samir,
  • Reham Hussein

摘要

Chronic kidney disorder is a rising danger to health that affects a significant percentage of older adults, and a crucial stage in its development is fibrosis. MicroRNAs and transforming_ growth factor-β1(TGF-β1) /SMAD2 signal pathway significantly regulate this process. miR-34a promotes extracellular matrix (ECM) deposition and inhibits B cell lymphoma-2 (Bcl-2), a target gene with antifibrotic properties shown to protect against renal fibrosis in animal models. Currently, several drugs, including entacapone, have been reported to suppress miR-34a activation. Experimental model of Carbon- tetrachloride (CCl4)-induced renal fibrosis revealed elevated serum levels of urea and creatinine, an increased urinary microalbumin-to-creatinine ratio, deterioration of the antioxidant-oxidant balance, an increase in TGF-β1 in renal tissue, and increased renal miR–34a–SMAD2 expression were observed, accompanied by decreased expression of Bcl-2. Entacapone holds reno-protective promises likely via its anti-inflammatory-antioxidant effects in CCl4-induced renal fibrosis by favorable modulation of miR-34a /TGF-β1/SMAD2 Signaling Pathway.