ArticleNature communications2018
Conditional deletion of Rcan1 predisposes to hypertension-mediated intramural hematoma and subsequent aneurysm and aortic rupture.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 16 citations in OpenAlex.
- Fibronectin-induced overactivation of αNature communications · 2026Article
- A Pathogenic ROCK-Signaling Network Involving a Lysine Deletion in Myh11 Renders Carriers Susceptible to Aortic Dissection.International journal of molecular sciences · 2026Article
- Novel insights into the association between organ damage and inflammatory response in preoperative abdominal aortic aneurysms.Frontiers in cardiovascular medicine · 2025Article
- Versican accumulation drives Nos2 induction and aortic disease in Marfan syndrome via Akt activation.EMBO molecular medicine · 2024Article
- Silicate ions as soluble form of bioactive ceramics alleviate aortic aneurysm and dissection.Bioactive materials · 2023Article
- Identification and validation of key genes associated with atrial fibrillation in the elderly.Frontiers in cardiovascular medicine · 2023Article
- RCAN1.4 suppresses the osteosarcoma growth and metastasis via interfering with the calcineurin/NFAT signaling pathway.Journal of bone oncology · 2021Article
- Review
- Aortic disease in Marfan syndrome is caused by overactivation of sGC-PRKG signaling by NO.Nature communications · 2021Article
- RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target.Molecular medicine (Cambridge, Mass.) · 2020Review
- Association of renal cyst and type A acute aortic dissection with hypertension.Journal of thoracic disease · 2020Article
- The RCAN1.4-calcineurin/NFAT signaling pathway is essential for hypoxic adaption of intervertebral discs.Experimental & molecular medicine · 2020Article
- Loss of Down syndrome critical region-1 leads to cholesterol metabolic dysfunction that exaggerates hypercholesterolemia in ApoE-null background.The Journal of biological chemistryArticle
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 at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aortic intramural hematoma (IMH) can evolve toward reabsorption, dissection or aneurysm. Hypertension is the most common predisposing factor in IMH and aneurysm patients, and the hypertensive mediator angiotensin-II induces both in mice. We have previously shown that constitutive deletion of Rcan1 isoforms prevents Angiotensin II-induced aneurysm in mice. Here we generate mice conditionally lacking each isoform or all isoforms in vascular smooth muscle cells, endothelial cells, or ubiquitously, to determine the contribution to aneurysm development of Rcan1 isoforms in vascular cells. Surprisingly, conditional Rcan1 deletion in either vascular cell-type induces a hypercontractile phenotype and aortic medial layer disorganization, predisposing to hypertension-mediated aortic rupture, IMH, and aneurysm. These processes are blocked by ROCK inhibition. We find that Rcan1 associates with GSK-3β, whose inhibition decreases myosin activation. Our results identify potential therapeutic targets for intervention in IMH and aneurysm and call for caution when interpreting phenotypes of constitutively and inducibly deficient mice.
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.