ReviewJournal of molecular medicine (Berlin, Germany)2025
The critical role of LRG1 in pathological fibrosis.
Review in Journal of molecular medicine (Berlin, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- LRG1 as a Potential Therapeutic Target in Atherosclerosis: Mechanistic Basis and Current Evidence.Cells · 2026Review
- Osteoactivin/GPNMB as a candidate biomarker of diabetic nephropathy in type 2 diabetes: associations with angiogenic and kidney injury biomarkers.Frontiers in endocrinology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Pathological fibrosis is a chronic process characterized by excessive deposition of extracellular matrix (ECM), which disrupts tissue architecture and function and accelerates disease progression in organs such as the lungs, liver, heart, kidneys, skin, and eyes. Recent studies have identified leucine-rich α-2 glycoprotein-1 (LRG1), a secreted glycoprotein known for modulating angiogenesis and immune responses, as a key player in the pathogenesis of fibrotic disorders. LRG1 expression is up-regulated by multiple pro-fibrotic mediators, including transforming growth factor-beta (TGF-β), and has been shown to regulate fibroblast differentiation, myofibroblast activation, and ECM production. Through interactions with the TGF-β signaling pathway and other cascades, LRG1 plays a crucial role in pathological fibrosis. Elucidating the molecular mechanisms by which LRG1 drives fibrogenic responses will pave the way for novel therapeutic strategies targeting pathological fibrosis. This review explores the emerging functions of LRG1 in fibrosis of different organs and discusses therapeutic approaches aimed at mitigating fibrosis through LRG1 inhibition.
Indexed as
Identifiers
What 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.