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<p>Bone morphogenetic protein 7 (BMP7) is a member of the transforming growth factor-β (TGF-β) superfamily and plays indispensable roles in embryonic kidney development, renal homeostasis, and tissue repair. In the adult kidney, BMP7 functions as an endogenous renoprotective factor through anti-inflammatory, anti-fibrotic, and regenerative mechanisms; however, its expression progressively declines with aging and chronic kidney injury. Increasing evidence suggests that disruption of the balance between BMP7 and profibrotic signaling pathways, particularly TGF-β1-associated signaling, contributes to the progression of kidney diseases. In experimental models, exogenous BMP7 supplementation or restoration of endogenous BMP7 activity attenuates inflammation, fibrosis, and functional deterioration in both acute and chronic kidney injury. In this review, we summarize the spatiotemporal expression patterns, canonical and non-canonical signaling pathways, and multilayer regulatory mechanisms governing BMP7 activity in the kidney. We further discuss the integrated roles of BMP7 in modulating inflammation, fibrosis, regenerative repair, and signaling crosstalk with key pathogenic pathways involved in kidney disease progression. In addition, we review current translational strategies targeting BMP7, including recombinant proteins, engineered delivery systems, and extracellular vesicle-associated approaches, together with the major challenges limiting clinical translation. Collectively, current evidence supports BMP7 as a promising but still incompletely understood therapeutic target in kidney diseases, warranting further mechanistic and translational investigation.</p>

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BMP7 in kidney development and disease: a multilayer regulatory network integrating inflammation, fibrosis, and regeneration

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月17日

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  • Heng Wang,
  • Yaling Li,
  • Guoping Zheng

摘要

Bone morphogenetic protein 7 (BMP7) is a member of the transforming growth factor-β (TGF-β) superfamily and plays indispensable roles in embryonic kidney development, renal homeostasis, and tissue repair. In the adult kidney, BMP7 functions as an endogenous renoprotective factor through anti-inflammatory, anti-fibrotic, and regenerative mechanisms; however, its expression progressively declines with aging and chronic kidney injury. Increasing evidence suggests that disruption of the balance between BMP7 and profibrotic signaling pathways, particularly TGF-β1-associated signaling, contributes to the progression of kidney diseases. In experimental models, exogenous BMP7 supplementation or restoration of endogenous BMP7 activity attenuates inflammation, fibrosis, and functional deterioration in both acute and chronic kidney injury. In this review, we summarize the spatiotemporal expression patterns, canonical and non-canonical signaling pathways, and multilayer regulatory mechanisms governing BMP7 activity in the kidney. We further discuss the integrated roles of BMP7 in modulating inflammation, fibrosis, regenerative repair, and signaling crosstalk with key pathogenic pathways involved in kidney disease progression. In addition, we review current translational strategies targeting BMP7, including recombinant proteins, engineered delivery systems, and extracellular vesicle-associated approaches, together with the major challenges limiting clinical translation. Collectively, current evidence supports BMP7 as a promising but still incompletely understood therapeutic target in kidney diseases, warranting further mechanistic and translational investigation.