ReviewMolecular biology reports2026
Potential role of CTHRC1 in renal fibrosis.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Renal fibrosis is a major morphological feature of chronic kidney disease and is considered an important pathogenetic process that leads to a decline in renal function in the progressive course of the disease. It is characterized by excessive accumulation of extracellular matrix, tubular atrophy, interstitial inflammation, capillary thinning, and nephron structural disruption. The development of fibrosis involves transforming growth factor-β (TGF-β), Wnt/β-catenin, inflammatory mediators, and intercellular communication between macrophages and activated fibroblasts. TGF-β, as one of the main driving factors of renal fibrosis, enhancing the activation of myofibroblasts and the accumulation of extracellular matrix proteins such as collagen and fibronectin through Smad-dependent and Smad-independent pathways. Collagen Triple Helix Repeat Containing 1 (CTHRC1), a secreted glycoprotein, was initially described in vascular remodeling and tissue repair processes after injury, and later studies began to consider it as a regulatory molecule in fibrotic diseases. The high expression of CTHRC1 protein in renal tissue in tubular cells and undetectable levels in glomerular cells provide a basis for investigating its association with tubulointerstitial injury in the kidney. CTHRC1 may be involved in fibroblast migration, tissue remodeling, extracellular matrix metabolism, and interaction with the TGF-β/Wnt signaling systems during kidney fibrogenesis. This review discusses the potential role of CTHRC1 in renal fibrosis, its relationship with the TGF-β and Wnt/β-catenin pathways, and its potential as a diagnostic biomarker and therapeutic target in chronic kidney diseases.
Indexed as
Identifiers
42886277What OpenQuestion holds
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.