ReviewJournal of cardiovascular development and disease2025
The Dual Role of ADAMTS1 in Cardiovascular Remodeling: Balancing Extracellular Matrix Homeostasis and Pathological States.
Review in Journal of cardiovascular development and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
2 authors.
Funding
Abstract
Extracellular matrix metalloproteinase ADAMTS1 (adhesion metalloproteinase with thrombospondin-type domain 1) is a key regulator in cardiovascular remodeling with functional paradoxes. This review synthesizes existing evidence to clarify its context-dependent dual roles across various cardiovascular diseases: on the one hand, ADAMTS1 exerts protective functions by maintaining vascular integrity and mitigating inflammatory responses; on the other hand, in conditions such as myocardial infarction and aortic aneurysms, ADAMTS1 promotes pathological progression by excessively hydrolyzing the multifunctional proteoglycan versican and other substrates, leading to tissue disruption and adverse remodeling. This functional switch in ADAMTS1 is jointly regulated by its cellular origin, temporal expression dynamics, and local microenvironment. In summary, ADAMTS1 represents a critical homeostasis node in the cardiovascular system. Therapeutic interventions targeting it should avoid broad-spectrum inhibition strategies; instead, future efforts should focus on developing precise, context-specific regulatory approaches.
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