ReviewKidney research and clinical practice2012
Smads as therapeutic targets for chronic kidney disease.
Review in Kidney research and clinical practice, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- The Ubiquitin-Specific Protease Family: Master Regulators of Renal Fibrosis Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2026Review
- An exploration of markers of microvascular dysfunction in kidney transplant recipients randomized to belatacept: no clinical impact of CNIs on endothelial function.Frontiers in transplantation · 2026Article
- Chromatin remodeling and epigenetic regulation in chronic kidney disease.Frontiers in genetics · 2026Review
- Integrative multi-omics profiling for early diagnosis, stratification and personalized management of chronic kidney disease: a new paradigm.Clinical and experimental medicine · 2025Review
- β-Mangostin Alleviates Renal Tubulointerstitial Fibrosis via the TGF-β1/JNK Signaling Pathway.Cells · 2024Article
- Retinoic acid receptor α activity in proximal tubules prevents kidney injury and fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Circulating extracellular vesicles in human cardiorenal syndrome promote renal injury in a kidney-on-chip system.JCI insight · 2023Article
- TGF-β Inhibitors for Therapeutic Management of Kidney Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Alterations in plasma miR-21, miR-590, miR-192 and miR-215 in idiopathic pulmonary fibrosis and their clinical importance.Molecular biology reports · 2022Article
- Shenkang Injection for Treating Renal Fibrosis-Metabonomics and Regulation of E3 Ubiquitin Ligase Smurfs on TGF-β/Smads Signal Transduction.Frontiers in pharmacology · 2022Article
- Case report: Focal segmental glomerulosclerosis in a pediatric atypical progeroid syndrome.Frontiers in pediatrics · 2022Article
- Transforming Growth Factor-β and Long Non-coding RNA in Renal Inflammation and Fibrosis.Frontiers in physiology · 2021Review
- Targeting the progression of chronic kidney disease.Nature reviews. Nephrology · 2020Review
- Identification of an activation-related protein in B cells in the ABO incompatible condition.Experimental and therapeutic medicine · 2020Article
- Effects of tranilast on the epithelial-to-mesenchymal transition in peritoneal mesothelial cells.Kidney research and clinical practice · 2019Article
- Astaxanthin ameliorates renal interstitial fibrosis and peritubular capillary rarefaction in unilateral ureteral obstruction.Molecular medicine reports · 2019Article
- Downregulation of microRNA-429 contributes to angiotensin II-induced profibrotic effect in rat kidney.American journal of physiology. Renal physiology · 2018Article
- Article
- Protective effect of yacon leaves extract (Research in pharmaceutical sciencesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis is a hallmark of chronic kidney disease (CKD). It is generally thought that transforming growth factor-β1 (TGF-β1) is a key mediator of fibrosis and mediates renal scarring positively by Smad2 and Smad3, but negatively by Smad7. Our recent studies found that in CKD, TGF-β1 is not a sole molecule to activate Smads. Many mediators such as angiotensin II and advanced glycation end products can also activate Smads via both TGF-β-dependent and independent mechanisms. In addition, Smads can interact with other signaling pathways, such as the mitogen-activated protein kinase and nuclear factor-kappaB (NF-κB) pathways, to regulate renal inflammation and fibrosis. In CKD, Smad2 and Smad3 are highly activated, while Smad7 is reduced or lost. In the context of fibrosis, Smad3 is pathogenic and mediates renal fibrosis by upregulating miR-21 and miR-192, but down-regulating miR-29 and miR-200 families. By contrast, Smad2 and Smad7 are protective. Overexpression of Smad7 inhibits both Smad3-mediated renal fibrosis and NF-κB-driven renal inflammation. Interestingly, Smad4 has diverse roles in renal fibrosis and inflammation. The complexity and distinct roles of individual Smads in CKD suggest that treatment of CKD should aim to correct the imbalance of Smad signaling or target the Smad3-dependent genes related to fibrosis, rather than to block the general effect of TGF-β1. Thus, treatment of CKD by overexpression of Smad7 or targeting Smad3-dependent miRNAs such as downregulation of miR-21 or overexpression of miR-29 may represent novel therapeutic strategies for CKD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.