ArticleFrontiers in molecular biosciences2026
Spinal cord injury-induced overflow incontinence reshapes the activin-follistatin-inhibin axis in mouse bladder and kidney.
Article in Frontiers in molecular biosciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Mesenchymal Stem Cell-Lysate Sustained-Release Nano-Hydrogel Alleviates Spinal Cord Injury by Inhibiting Ferroptosis and Mitochondrial Intrinsic Apoptosis.International dental journal · 2026Article
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6 authors.
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Abstract
Background: Spinal cord injury is a leading cause of neurogenic bladder and upper urinary tract deterioration, yet the molecular remodeling of epithelial-stromal signaling axes in this context remains incompletely defined. The activin-follistatin-inhibin axis, a branch of the transforming growth factor-β superfamily, has been implicated in tissue repair, inflammation, and fibrosis, but its behavior in the lower urinary tract after SCI is unknown. Methods: A standardized T9-T10 contusion SCI model was established in male C57BL/6J mice. Bladder dysfunction was assessed using the voiding spot assay. Gross morphology and organ weights of the bladder and kidneys were recorded. Quantitative RT-PCR was used to profile mRNA expression of 11 AFI-axis genes in bladder and kidney. Western blotting was performed for selected proteins, and immunofluorescence was used to map the spatial distribution of FST, INHA and INHBE in bladder and INHA, INHBB and INHBE in kidney. Results: SCI mice displayed numerous irregular urine spots with leakage/tailing on the voiding spot assay and an increased voided area, accompanied by marked bladder distension and increased bladder and kidney weights compared with sham controls, suggesting compromised voiding efficiency and impaired bladder emptying. In the bladder, Conclusion: SCI reshapes the AFI axis in both bladder and kidney, characterized by coordinated but regionally distinct alterations in FST, INHA, INHBE, and INHBB expression. These findings extend the concept that the AFI axis contributes to urothelial-stromal homeostasis and suggest that AFI-axis remodeling is part of the molecular signature of neurogenic bladder and associated renal adaptation after SCI. These observational findings nominate the AFI axis as a priority pathway for future mechanistic and interventional evaluation, with therapeutic potential to be determined using objective functional endpoints.
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