ArticleKidney international2018
The activin receptor is stimulated in the skeleton, vasculature, heart, and kidney during chronic kidney disease.
Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 61 citations in OpenAlex.
- Iron, ESA, and HIF-Inhibitors: Are There Other Opportunities to Improve Anemia of CKD?Journal of clinical medicine · 2026Review
- Serum activin A and bone metabolism in patients undergoing hemodialysis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Article
- A Western Diet High in Phosphate Primes the Development of the CKD-Mineral Bone Disorder in an Alport Syndrome Model.Kidney360 · 2026Article
- Advances in noninvasive diagnosis of renal osteodystrophy.Renal failure · 2025Review
- Collagen IV in Gould syndrome and Alport syndrome.Nature reviews. Nephrology · 2025Review
- Targeting casein kinase 2 and ubiquitin-specific protease 7 to modulate RUNX2-mediated osteogenesis in chronic kidney disease.Molecular medicine (Cambridge, Mass.) · 2025Article
- Sotatercept: A Crosstalk Between Pathways and Activities in the Pulmonary Circulation and Blood.International journal of molecular sciences · 2025Review
- Interplay between Skeletal Muscle Catabolism and Remodeling of Arteriovenous Fistula by Yes-Associated Protein 1 (YAP1) Signaling.Journal of the American Society of Nephrology : JASN · 2025Article
- Article
- Bone-organ axes: bidirectional crosstalk.Military Medical Research · 2024Review
- In chronic kidney disease altered cardiac metabolism precedes cardiac hypertrophy.American journal of physiology. Renal physiology · 2024Article
- Advances in sarcopenia: mechanisms, therapeutic targets, and intervention strategies.Archives of pharmacal research · 2024Review
- Plasma activin A rises with declining kidney function and is independently associated with mortality in patients with chronic kidney disease.Clinical kidney journal · 2023Article
- Mouse Models of Mineral Bone Disorders Associated with Chronic Kidney Disease.International journal of molecular sciences · 2023Review
- Updates in the chronic kidney disease-mineral bone disorder show the role of osteocytic proteins, a potential mechanism of the bone-Vascular paradox, a therapeutic target, and a biomarker.Frontiers in physiology · 2023Review
- The Growth Factors: Potential Biomarkers and Therapeutic Targets in Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2022Review
- Emerging cross-talks between chronic kidney disease-mineral and bone disorder (CKD-MBD) and malnutrition-inflammation complex syndrome (MICS) in patients receiving dialysis.Clinical and experimental nephrology · 2022Review
- Elevated TGFβ signaling contributes to ocular anterior segment dysgenesis in Col4a1 mutant mice.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- The Calcified Vasculature in Chronic Kidney Disease Secretes Factors that Inhibit Bone Mineralization.JBMR plus · 2022Article
- Single-Cell Transcriptome Analysis Reveals Embryonic Endothelial Heterogeneity at Spatiotemporal Level and Multifunctions of MicroRNA-126 in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We examined activin receptor type IIA (ActRIIA) activation in chronic kidney disease (CKD) by signal analysis and inhibition in mice with Alport syndrome using the ActRIIA ligand trap RAP-011 initiated in 75-day-old Alport mice. At 200 days of age, there was severe CKD and associated Mineral and Bone Disorder (CKD-MBD), consisting of osteodystrophy, vascular calcification, cardiac hypertrophy, hyperphosphatemia, hyperparathyroidism, elevated FGF23, and reduced klotho. The CKD-induced bone resorption and osteoblast dysfunction was reversed, and bone formation was increased by RAP-011. ActRIIA inhibition prevented the formation of calcium apatite deposits in the aortic adventitia and tunica media and significantly decreased the mean aortic calcium concentration from 0.59 in untreated to 0.36 mg/g in treated Alport mice. Aortic ActRIIA stimulation in untreated mice increased p-Smad2 levels and the transcription of sm22α and αSMA. ActRIIA inhibition reversed aortic expression of the osteoblast transition markers Runx2 and osterix. Heart weight was significantly increased by 26% in untreated mice but remained normal during RAP-011 treatment. In 150-day-old mice, GFR was significantly reduced by 55%, but only by 30% in the RAP-011-treated group. In 200-day-old mice, the mean BUN was 100 mg/dl in untreated mice compared to 60 mg/dl in the treated group. In the kidneys of 200-day-old mice, ActRIIA and p-Smad2 were induced and MCP-1, fibronectin, and interstitial fibrosis were stimulated; all were attenuated by RAP-011 treatment. Hence, the activation of ActRIIA signaling during early CKD contributes to the CKD-MBD components of osteodystrophy and cardiovascular disease and to renal fibrosis. Thus, the inhibition of ActRIIA signaling is efficacious in improving and delaying CKD-MBD in this model of Alport syndrome.
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