ReviewInternational urology and nephrology2015
Role of Smad signaling in kidney disease.
Review in International urology and nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
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
21 citing papers in PubMed, 39 citations in OpenAlex.
- Genetic contributions to lupus nephritis in a multi-ethnic cohort of systemic lupus erythematous patients.PloS one · 2018Trial
- Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2025Review
- Eucommiae cortex extract alleviates renal fibrosis in CKD mice induced by adenine through the TGF-β1/Smad signaling pathway.Journal of natural medicines · 2025Article
- Inhibin subunit beta B (INHBB): an emerging role in tumor progression.Journal of physiology and biochemistry · 2024Review
- Potentials of Natural Antioxidants in Reducing Inflammation and Oxidative Stress in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- ELABELA-derived peptide ELA13 attenuates kidney fibrosis by inhibiting the Smad and ERK signaling pathways.Journal of Zhejiang University. Science. B · 2024Article
- Urinary Excretion of Biomolecules Related to Cell Cycle, Proliferation, and Autophagy in Subjects with Type 2 Diabetes and Chronic Kidney Disease.Biomedicines · 2024Article
- Randomized Trial of SGLT2 Inhibitor Identifies Target Proteins in Diabetic Kidney Disease.Kidney international reports · 2024Article
- Comprehensive single-cell transcriptional profiling defines shared and unique epithelial injury responses during kidney fibrosis.Cell metabolism · 2022Article
- Mitochondrial Pathophysiology on Chronic Kidney Disease.International journal of molecular sciences · 2022Review
- Corni Fructus Alleviates UUO-Induced Renal Fibrosis via TGF-BioMed research international · 2022Article
- Shen-Shuai-Ling Formulation Attenuates Renal Interstitial Fibrosis in Chronic Kidney Disease by Regulating SHH-Gli1 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Article
- Remdesivir Inhibits Tubulointerstitial Fibrosis in Obstructed Kidneys.Frontiers in pharmacology · 2021Article
- Retracted Article: TMEM88 inhibits fibrosis in renal proximal tubular epithelial cells by suppressing the transforming growth factor-β1/Smad signaling pathway.RSC advances · 2019Article
- miR-134 inhibits chondrogenic differentiation of bone marrow mesenchymal stem cells by targetting SMAD6.Bioscience reports · 2019Article
- 3,3'-Diindolylmethane ameliorates renal fibrosis through the inhibition of renal fibroblast activation in vivo and in vitro.Renal failure · 2018Article
- Altering equine corneal fibroblast differentiation through Smad gene transfer.Veterinary ophthalmology · 2018Article
- Risk factors in Swedish young men for amyotrophic lateral sclerosis in adulthood.Journal of neurology · 2018Article
- Interleukin-17 induces human alveolar epithelial to mesenchymal cell transition via the TGF-β1 mediated Smad2/3 and ERK1/2 activation.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smads are the key intermediates of canonical transforming growth factor-beta (TGF-β) signaling. These intermediates are divided into three distinct subgroups based on their role in TGF-β family signal transduction: Receptor-regulated Smads (R-Smads) 1, 2, 3, 5 and 8, common Smad4, and inhibitory Smads6 and 7. TGF-β signaling through Smad pathway involves phosphorylation, ubiquitination, sumoylation, acetylation, and protein-protein interactions with mitogen-activated protein kinases, PI3K-Akt/PKB, and Wnt/GSK-3. Several studies have suggested that upregulation or downregulation of TGF-β/Smad signaling pathways may be a pathogenic mechanism in the progression of chronic kidney disease. Smad2 and 3 are the two major downstream R-Smads in TGF-β-mediated renal fibrosis, while Smad7 also controls renal inflammation. In this review, we characterize the role of Smads in kidney disease, describe the molecular mechanisms, and discuss the potential of Smads as a therapeutic target in chronic kidney disease.
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Registered trials
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.