ArticleiScience2021
Therapeutic silencing of SMOC2 prevents kidney function loss in mouse model of chronic kidney disease.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- SMOC2 promotes partial epithelial-mesenchymal transition and maladaptive repair in renal tubular epithelial cells.JCI insight · 2026Article
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- Proteomics approach identifies aqueous humor biomarkers in retinal diseases.Communications medicine · 2025Article
- Permanent defects in renal medullary structure and function after reversal of urinary obstruction.JCI insight · 2025Article
- Uncovering hub genes and immunological characteristics for heart failure utilizing RRA, WGCNA and Machine learning.International journal of cardiology. Heart & vasculature · 2024Article
- Plasma SMOC2 Predicts Prognosis in Patients with Heart Failure: A Prospective Cohort.International journal of general medicine · 2024Article
- SMOC2 plays a role in heart failure via regulating TGF-β1/Smad3 pathway-mediated autophagy.Open medicine (Warsaw, Poland) · 2023Article
- Suppression of SMOC2 alleviates myocardial fibrosisFrontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
Chronic kidney disease (CKD) is associated with substantial morbidity and mortality. We developed a mouse model that mimics human CKD with inflammation, extracellular matrix deposition, tubulointerstitial fibrosis, increased proteinuria, and associated reduction in glomerular filtration rate over time. Using this model, we show that genetic deficiency of SMOC2 or therapeutic silencing of SMOC2 with small interfering RNAs (siRNAs) after disease onset significantly ameliorates inflammation, fibrosis, and kidney function loss. Mechanistically, we found that SMOC2 promotes fibroblast to myofibroblast differentiation by activation of diverse cellular signaling pathways including MAPKs, Smad, and Akt. Thus, targeting SMOC2 therapeutically offers an approach to prevent fibrosis progression and CKD after injury.
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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.