ReviewInternational journal of molecular sciences2018
Systemic Activation of Activin A Signaling Causes Chronic Kidney Disease-Mineral Bone Disorder.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Mineral and Bone Disease in CKD and Kidney Transplantation: Controversies, Gaps, and a Path Forward.Kidney international reports · 2026Review
- 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
- Advances in noninvasive diagnosis of renal osteodystrophy.Renal failure · 2025Review
- Targeting casein kinase 2 and ubiquitin-specific protease 7 to modulate RUNX2-mediated osteogenesis in chronic kidney disease.Molecular medicine (Cambridge, Mass.) · 2025Article
- Molecular pathophysiology of chronic kidney disease-mineral and bone disorder: Focus on the fibroblast growth factor 23-Klotho axis and bone turnover dynamics.Experimental physiology · 2025Review
- Circulating Muscle Markers for Sarcopenia in Peritoneal Dialysis.International journal of nephrology · 2025Review
- Development of animal models with chronic kidney disease-mineral and bone disorder based on clinical characteristics and pathogenesis.Frontiers in endocrinology · 2025Review
- Activin A: a marker of mineral bone disorder in children with chronic kidney disease?Pediatric nephrology (Berlin, Germany) · 2024Article
- Activin A, a Novel Chemokine, Induces Mouse NK Cell Migration via AKT and Calcium Signaling.Cells · 2024Article
- Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway.Oncology reports · 2024Article
- COVID-19 and Bone Loss: A Review of Risk Factors, Mechanisms, and Future Directions.Current osteoporosis reports · 2024Review
- SARS-CoV-2 and its Multifaceted Impact on Bone Health: Mechanisms and Clinical Evidence.Current osteoporosis reports · 2024Review
- Osteoporosis treatment: current drugs and future developments.Frontiers in pharmacology · 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
- Maternal Low Volume Circulation Relates to Normotensive and Preeclamptic Fetal Growth Restriction.Frontiers in medicine · 2022Review
- The association between serum activin A levels and albuminuria among community-dwelling middle-aged and older adults in Taiwan.Scientific reports · 2021Article
- Review
- The Influence of Dietary Interventions on Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD).Nutrients · 2021Review
- Preeclampsia Is a Syndrome with a Cascade of Pathophysiologic Events.Journal of clinical medicine · 2020Review
- New Markers of Renal Failure in Multiple Myeloma and Monoclonal Gammopathies.Journal of clinical medicine · 2020Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high cardiovascular mortality associated with chronic kidney disease (CKD) is caused in part by the CKD-mineral bone disorder (CKD-MBD) syndrome. The CKD-MBD consists of skeletal, vascular and cardiac pathology caused by metabolic derangements produced by kidney disease. The prevalence of osteopenia/osteoporosis resulting from the skeletal component of the CKD-MBD, renal osteodystrophy (ROD), in patients with CKD exceeds that of the general population and is a major public health concern. That CKD is associated with compromised bone health is widely accepted, yet the mechanisms underlying impaired bone metabolism in CKD are not fully understood. Therefore, clarification of the molecular mechanisms by which CKD produces ROD is of crucial significance. We have shown that activin A, a member of the transforming growth factor (TGF)-β super family, is an important positive regulator of receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis with Smad-mediated signaling being crucial for inducing osteoclast development and function. Recently, we have demonstrated systemic activation of activin receptors and activin A levels in CKD mouse models, such as diabetic CKD and Alport (AL) syndrome. In these CKD mouse models, bone remodeling caused by increased osteoclast numbers and activated osteoclastic bone resorption was observed and treatment with an activin receptor ligand trap repaired CKD-induced-osteoclastic bone resorption and stimulated individual osteoblastic bone formation, irrespective of
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