ArticlePloS one2020
Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Kindlin-2 Deletion in Mural Cells Leads to Vascular Instability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Paxillin and Kindlin: Research Progress and Biological Functions.Biomolecules · 2025Review
- FAK Family Kinases: A Potential Therapeutic Target for Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Article
- Role of advanced glycation end products on vascular smooth muscle cells under diabetic atherosclerosis.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular hyperplasia after vascular trauma is one of the difficult problems in clinical treatment. Nowadays, there is no effective treatment for vascular hyperplasia. Previous studies have shown that integrinβ1 andβ3 activity play an important role in vascular hyperplasia. Kindlin-2 has been shown to modulate integrinβ1 andβ3 activity in cancer. Therefore, in this study, we hope to explore the relationship between Kindlin-2 and vascular hyperplasia. We overexpressed or knocked down Kindlin-2 by adenovirus. The results showed that Kindlin-2 overexpression could regulate integrinβ1 andβ3 activity through FAK-PIK3 signaling pathways ex vivo and in vivo, thereby affecting the proliferation and migration of VSMC, and then it causes the consequences of vascular hyperplasia. Therefore, Our results show that Kindlin-2 may be a potential target for the treatment of vascular hyperplasia.
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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.