ArticleBiomedical reports2019
Crim1 suppresses left ventricular hypertrophy.
Article in Biomedical reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Integrated multiomics of pressure overload in the human heart prioritizes targets relevant to heart failure.Nature communications · 2025Article
- Crim1 inhibits angiotensin II-induced hypertrophy and preserves Kv4.2 expression in cardiomyocytes.Iranian journal of basic medical sciences · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Left ventricular hypertrophy is a leading cause of heart failure and sudden death. Cysteine-rich transmembrane bone morphogenetic protein regulator 1 (Crim1) is expressed at a high level in the heart and has a regulatory role in heart development. The present study aimed to test the hypothesis that Crim1 can have an inhibitory function on ventricular hypertrophy. Rat primary ventricular myocytes were stretched to induce myocyte hypertrophy, and treated with telmisartan or infected with Crim1-expressing recombinant adenovirus (Ad-Crim1). Rat ventricular hypertrophy was induced by abdominal aortic coarctation (AAC), and treated either with telmisartan or myocardial injection of Ad-Crim1 or empty adenovirus vector. The results showed that the expression of Crim1 decreased in the hypertrophic ventricle. The inhibition of angiotensin receptor type 1 (AT1R) by telmisartan
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