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<p>Renal inflammation, oxidative stress, and fibrosis are hallmarks of kidney diseases, including diabetic nephropathy, acute kidney injury (AKI), and chronic kidney disease (CKD). The global prevalence of kidney diseases is increasing, posing a substantial public health challenge. The pathophysiology of kidney diseases is complex and multifactorial, involving a dynamic interplay of oxidative stress, inflammation, and fibrosis. Persistent inflammation in CKD is driven by elevated levels of proinflammatory mediators such as interleukin-6 (IL-6), interleukin-1beta (IL-1β), and tumor necrosis factor-alpha (TNF-α). Elevated C-reactive protein (CRP) levels are commonly associated with AKI and CKD. Moreover, oxidative stress, due to increased reactive oxygen species (ROS) and diminished antioxidant defenses, further damages renal tissues. Additionally, renal fibrosis mediated by transforming growth factor beta (TGF-β) signaling contributes to progressive structural deterioration, ultimately leading to end-stage kidney disease. Given the multifactorial nature of kidney disease, driven by the complex interplay of various mediators, there is a need for compounds with multitargeting potential. Formononetin (7-hydroxy-4’-methoxyisoflavone) is a naturally occurring isoflavone known for its broad pharmacological profile, including anti-inflammatory, antioxidant, renoprotective, cardioprotective, and antidiabetic activity. Various studies have demonstrated the significant potential of formononetin in mitigating kidney diseases through the modulation of multiple molecular mediators, including p38-mitogen-activated protein kinase (p38-MAPK), janus kinase (JNK), TGF-β, nuclear factor kappa B (NF-κB), CRP, sirtuin 1 (SIRT1), proinflammatory cytokines, nuclear factor erythroid 2-related factor 2 (Nrf-2), kelch-like ECH-associated protein 1 (Keap1), antioxidants, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX). Given formononetin’s ability to modulate key molecular mediators involved in kidney disease, this review aims to explore the underlying mechanisms driving its renoprotective effects. By examining these complex and interconnected pathways, the review seeks to provide essential insights that will guide future research and help bridge existing knowledge gaps regarding formononetin’s potential in renal disorders.</p>

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Formononetin as a multifaceted modulator of renal pathology: insights into fibrotic, oxidative, inflammatory, and apoptotic pathways

  • 期刊论文

  • 发表日期：

    2025年10月28日

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  • Anish Singh,
  • Lovedeep Singh,
  • Diksha Dalal

摘要

Renal inflammation, oxidative stress, and fibrosis are hallmarks of kidney diseases, including diabetic nephropathy, acute kidney injury (AKI), and chronic kidney disease (CKD). The global prevalence of kidney diseases is increasing, posing a substantial public health challenge. The pathophysiology of kidney diseases is complex and multifactorial, involving a dynamic interplay of oxidative stress, inflammation, and fibrosis. Persistent inflammation in CKD is driven by elevated levels of proinflammatory mediators such as interleukin-6 (IL-6), interleukin-1beta (IL-1β), and tumor necrosis factor-alpha (TNF-α). Elevated C-reactive protein (CRP) levels are commonly associated with AKI and CKD. Moreover, oxidative stress, due to increased reactive oxygen species (ROS) and diminished antioxidant defenses, further damages renal tissues. Additionally, renal fibrosis mediated by transforming growth factor beta (TGF-β) signaling contributes to progressive structural deterioration, ultimately leading to end-stage kidney disease. Given the multifactorial nature of kidney disease, driven by the complex interplay of various mediators, there is a need for compounds with multitargeting potential. Formononetin (7-hydroxy-4’-methoxyisoflavone) is a naturally occurring isoflavone known for its broad pharmacological profile, including anti-inflammatory, antioxidant, renoprotective, cardioprotective, and antidiabetic activity. Various studies have demonstrated the significant potential of formononetin in mitigating kidney diseases through the modulation of multiple molecular mediators, including p38-mitogen-activated protein kinase (p38-MAPK), janus kinase (JNK), TGF-β, nuclear factor kappa B (NF-κB), CRP, sirtuin 1 (SIRT1), proinflammatory cytokines, nuclear factor erythroid 2-related factor 2 (Nrf-2), kelch-like ECH-associated protein 1 (Keap1), antioxidants, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX). Given formononetin’s ability to modulate key molecular mediators involved in kidney disease, this review aims to explore the underlying mechanisms driving its renoprotective effects. By examining these complex and interconnected pathways, the review seeks to provide essential insights that will guide future research and help bridge existing knowledge gaps regarding formononetin’s potential in renal disorders.