ArticleJournal of vascular surgery2015
Hypercholesterolemia inhibits re-endothelialization of arterial injuries by TRPC channel activation.
Article in Journal of vascular surgery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Genetic ablation of TRPC6 facilitated age-dependent atherosclerosis progression in an ApoE-/- mouse model.Frontiers in physiology · 2026Article
- Article
- TRPC5 channel participates in myocardial injury in chronic intermittent hypoxia.Clinics (Sao Paulo, Brazil) · 2024Article
- iPLA2 inhibition blocks LysoPC-induced TRPC6 externalization and promotes Re-endothelialization of carotid injuries in hypercholesterolemic mice.Cell calcium · 2023Article
- p38 MAPK activation and STIM1-Orai3 association mediate TRPC6 externalization.American journal of physiology. Cell physiology · 2023Article
- p85α regulatory subunit isoform controls PI3-kinase and TRPC6 membrane translocation.Cell calcium · 2023Article
- TRPC5 as a possible therapeutic target for vascular dysfunction associated with obesity.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Article
- Inhibition of P110α and P110δ catalytic subunits of PI3 kinase reverses impaired arterial healing after injury in hypercholesterolemic male mice.American journal of physiology. Cell physiology · 2021Article
- P110α and P110δ catalytic subunits of PI3 kinase regulate lysophosphatidylcholine-induced TRPC6 externalization.American journal of physiology. Cell physiology · 2021Article
- Review
- Transient receptor potential cation channel subfamily C member 6 participates in functional regulation of vascular smooth muscle cells.JVS-vascular science · 2020Article
- Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury.JVS-vascular science · 2020Article
- Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular CaFrontiers in physiology · 2019Review
- TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular CaThe journal of physiological sciences : JPS · 2018Article
- Integration of TRPC6 and NADPH oxidase activation in lysophosphatidylcholine-induced TRPC5 externalization.American journal of physiology. Cell physiology · 2017Article
- Canonical Transient Receptor Potential Channels and Their Link with Cardio/Cerebro-Vascular Diseases.Biomolecules & therapeutics · 2017Review
- Membrane translocation of TRPC6 channels and endothelial migration are regulated by calmodulin and PI3 kinase activation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Apolipoprotein A-I mimetic peptide reverses impaired arterial healing after injury by reducing oxidative stress.Atherosclerosis · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAfter arterial injury, endothelial cell (EC) migration is essential for healing, but lipid oxidation products activate TRPC6 and TRPC5 ion channels, leading to increased intracellular calcium and inhibition of EC migration in vitro. The objective of this study was to further evaluate the role of TRPC channels in EC migration in vitro and to validate in vitro findings in an in vivo model.
methodsMouse aortic ECs were cultured, and the effect of lysophosphatidylcholine, the major lysophospholipid in oxidized low-density lipoprotein, on migration was assessed in a razor-scrape assay. EC healing after a carotid injury with electrocautery was evaluated in wild-type (WT), TRPC6(-/-), and TRPC5(-/-) mice receiving either a chow or high-cholesterol (HC) diet.
resultsLysophosphatidylcholine inhibited EC migration of WT ECs to 22% of baseline and of TRPC5(-/-) ECs to 53% of baseline but had minimal effect on TRPC6(-/-) EC migration. Hypercholesterolemia severely impaired EC healing in vivo, with 51.4% ± 1.8% and 24.9% ± 2.0% of the injury resurfaced with ECs at 5 days in chow-fed and HC-fed WT mice, respectively (P < .001). Hypercholesterolemia did not impair healing in TRPC6(-/-) mice, with coverage of 48.4% ± 3.4% and 46.8% ± 1.6% in chow-fed and HC-fed TRPC6(-/-) mice, respectively. Hypercholesterolemia had a reduced inhibitory effect in TRPC5(-/-) mice, with EC coverage of 51.7% ± 3.0% and 37.% ± 1.4% in chow-fed and HC-fed TRPC5(-/-) mice, respectively.
conclusionsResults suggest that activation of TRPC6 and TRPC5 channels is the key contributor to impaired endothelial healing of arterial injuries in hypercholesterolemic 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.