ArticleBioMed research international2014
Follistatin, an activin antagonist, ameliorates renal interstitial fibrosis in a rat model of unilateral ureteral obstruction.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Activin A: a novel urinary biomarker of renal impairment in multiple myeloma.Bioscience reports · 2019Trial
- Clinical Anterior Segment and Ocular Surface Findings Across Renal Replacement Modalities: Associations with CKD-Related Factors, Mineral Metabolism and Activin A.Life (Basel, Switzerland) · 2026Article
- Smad2/3 Signaling Mediates the Atrophic Response in Vocal Fold Myoblasts In Vitro.The Laryngoscope · 2026Article
- ECM formation and degradation during fibrosis, repair, and regeneration.npj metabolic health and disease · 2025Review
- Article
- Follistatin lowers blood pressure and improves vascular structure and function in essential and secondary hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Cytokine priming enhances the antifibrotic effects of human adipose derived mesenchymal stromal cells conditioned medium.Stem cell research & therapy · 2024Article
- Plasma activin A rises with declining kidney function and is independently associated with mortality in patients with chronic kidney disease.Clinical kidney journal · 2023Article
- Circulating extracellular vesicles in human cardiorenal syndrome promote renal injury in a kidney-on-chip system.JCI insight · 2023Article
- Article
- A therapeutic target for CKD: activin A facilitates TGFβ1 profibrotic signaling.Cellular & molecular biology letters · 2023Article
- The Growth Factors: Potential Biomarkers and Therapeutic Targets in Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2022Review
- Neuroblastoma suppressor of tumorigenicity 1 is a circulating protein associated with progression to end-stage kidney disease in diabetes.Science translational medicine · 2022Article
- Urinary Activin A: A Novel Biomarker for Human Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2022Article
- Causal contributors to tissue stiffness and clinical relevance in urology.Communications biology · 2021Review
- miR299a-5p promotes renal fibrosis by suppressing the antifibrotic actions of follistatin.Scientific reports · 2021Article
- Androgen-Influenced Polarization of Activin A-Producing Macrophages Accompanies Post-pyelonephritic Renal Scarring.Frontiers in immunology · 2020Article
- Circadian rhythm of activin A and related parameters of mineral metabolism in normal and uremic rats.Pflugers Archiv : European journal of physiology · 2019Article
- Caveolin-1 regulation of Sp1 controls production of the antifibrotic protein follistatin in kidney mesangial cells.Cell communication and signaling : CCS · 2019Article
- Follistatin Effects in Migration, Vascularization, and OsteogenesisFrontiers in bioengineering and biotechnology · 2019Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activin, a member of the TGF-β superfamily, regulates cell growth and differentiation in various cell types. Activin A acts as a negative regulator of renal development as well as tubular regeneration after renal injury. However, it remains unknown whether activin A is involved in renal fibrosis. To clarify this issue, we utilized a rat model of unilateral ureteral obstruction (UUO). The expression of activin A was significantly increased in the UUO kidneys compared to that in contralateral kidneys. Activin A was detected in glomerular mesangial cells and interstitial fibroblasts in normal kidneys. In UUO kidneys, activin A was abundantly expressed by interstitial α-SMA-positive myofibroblasts. Administration of recombinant follistatin, an activin antagonist, reduced the fibrotic area in the UUO kidneys. The number of proliferating cells in the interstitium, but not in the tubules, was significantly lower in the follistatin-treated kidneys. Expression of α-SMA, deposition of type I collagen and fibronectin, and CD68-positive macrophage infiltration were significantly suppressed in the follistatin-treated kidneys. These data suggest that activin A produced by interstitial fibroblasts acts as a potent profibrotic factor during renal fibrosis. Blockade of activin A action may be a novel approach for the prevention of renal fibrosis progression.
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