Bone Morphogenetic Protein-7 in Kidney Injury and Repair
Summary
Bone Morphogenetic Protein-7 (BMP-7) is a multifunctional growth factor of the transforming growth factor-β (TGF-β) superfamily that plays a pivotal role in renal development, maintenance of tubular architecture and response to injury. In healthy kidneys, BMP-7 maintains epithelial phenotype, counterbalances profibrotic TGF-β signalling and supports cellular plasticity. Following acute or chronic insult—from ischaemia, toxins or metabolic stress—BMP-7 expression declines, coinciding with epithelial–mesenchymal transition (EMT), excessive extracellular matrix (ECM) deposition and progressive fibrosis. Restoration of BMP-7 activity promotes mesenchymal–epithelial transition (MET) in interstitial fibroblasts, reduces apoptotic and ferroptotic cell death of tubular epithelia and suppresses inflammatory cascades. Together, these effects accelerate tubular repair, limit scar formation and preserve glomerular and tubular function. Preclinical studies have illustrated that exogenous BMP-7 or delivery of stabilised BMP-7 formulations can reverse established fibrosis in animal models, highlighting its therapeutic potential across a spectrum of kidney injuries.
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Bone Morphogenetic Protein-7 in Kidney Injury and Repair publication trend
The graph below shows the total number of articles in bone morphogenetic protein-7 in kidney injury and repair across all publications each year (not limited to Nature Index journals).
Technical terms
Bone Morphogenetic Protein-7 (BMP-7): A morphogen of the TGF-β superfamily essential for renal development and repair.
Transforming Growth Factor-β (TGF-β): A cytokine that drives fibrogenesis and EMT in injured tissues.
Epithelial–Mesenchymal Transition (EMT): A process by which epithelial cells acquire fibroblast-like properties, contributing to fibrosis.
Mesenchymal–Epithelial Transition (MET): The reverse process of EMT, enabling fibroblasts to regain epithelial characteristics and support tissue repair.
Extracellular Matrix (ECM): The network of proteins and polysaccharides that provides structural support to cells; excessive deposition leads to scarring.
Ferroptosis: Iron-dependent cell death characterised by lipid peroxidation, implicated in acute and chronic renal injury.
Smad Proteins: Intracellular mediators of TGF-β and BMP signals; Smad1/5 transduce BMP-7 signals, whereas Smad2/3 convey TGF-β signals.
SnoN: A transcriptional co-repressor regulated by BMP-7/Smad1/5 that inhibits profibrotic gene expression.
References
- Bone morphogenetic protein-7 attenuates pancreatic damage under diabetic conditions and prevents progression to diabetic nephropathy via inhibition of ferroptosis. Frontiers in Endocrinology (2023).
- Bone Morphogenic Protein-7 Induces Mesenchymal to Epithelial Transition in Adult Renal Fibroblasts and Facilitates Regeneration of Injured Kidney*. Journal of Biological Chemistry (2004).
- Role of bone morphogenetic protein-7 in renal fibrosis. Frontiers in Physiology (2015).
- BMP-7 ameliorates partial epithelial-mesenchymal transition by restoring SnoN protein level via Smad1/5 pathway in diabetic kidney disease. Cell Death & Disease (2022).
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