Evidence map›Paper›PMID 26940997›Full record

ArticleActa biochimica et biophysica Sinica2016

Atorvastatin blocks increased l-type Ca2+ current and cell injury elicited by angiotensin II via inhibiting oxide stress.

Yanzhuo Ma, Lingfeng Kong, Shuying Qi, Dongmei Wang

Open access · bronzeAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 20% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Mitochondrial Calcium Uniporter-Mediated Regulation of the SIRT3/GSK3β/β-Catenin Signaling Pathway in Vascular Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  3. Review
  4. Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Yanzhuo MaDepartment of Cardiology, Bethune International Peace Hospital, Shijiazhuang 050000, China.
Lingfeng KongDepartment of Cardiology, Bethune International Peace Hospital, Shijiazhuang 050000, China Hebei Medical University, Shijiazhuang 050011, China.
Shuying QiDepartment of Cardiology, Bethune International Peace Hospital, Shijiazhuang 050000, China.
Dongmei WangDepartment of Cardiology, Bethune International Peace Hospital, Shijiazhuang 050000, China slwangdm@126.com.
Bethune International Peace Hospital · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thel-type Ca(2+)current (ICa,l) plays a crucial role in shaping action potential and is involved in cardiac arrhythmia. Statins have been demonstrated to contribute to anti-apoptotic and anti-arrhythmic effects in the heart. Here, we examined whether atorvastatin regulates theICa,land cell injury induced by angiotensin II (AngII) as well as the putative intracellular cascade responsible for the effects. Cultured neonatal rat ventricular myocytes were incubated with AngII for 24 h, and then cell injury and expression levels of Nox2/gp91(phox), p47(phox) ,and Cav1.2 were analyzed. In addition,ICa,lwas recorded using the whole-cell patch-clamp technique, and mechanisms of atorvastatin actions were also investigated. It was found that the number of apoptotic cardiomyocytes was increased and cell viability was significantly decreased after AngII administration. AngII also augmented the expressions of Nox2/gp91(phox)and p47(phox)compared with control cardiomyocytes. Exposure to AngII evokedICa,lin a voltage-dependent manner without affecting theI-Vrelationship. In addition, AngII enhanced membrane Cav1.2 expression. These effects were abolished in the presence of the reactive oxygen species (ROS) scavenger, manganese (III)-tetrakis 4-benzoic acid porphyrin [Mn(III)TBAP], or the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, atorvastatin. These results suggested that atorvastatin mediates cardioprotection against arrhythmias and cell injury by controlling the AngII-ROS cascade.

Indexed as

Angiotensin IIAnimalsAnimals, NewbornAtorvastatinCalcium Channels, L-TypeCell LineHydroxymethylglutaryl-CoA Reductase InhibitorsOxidative StressRatsRats, Sprague-DawleyReactive Oxygen SpeciesAngiotensin IIAtorvastatinCalcium Channels, L-TypeHydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen Speciesangiotensin IIapoptosisatorvastatinl-type Ca2+ current

Identifiers

PMID26940997
PMCPMC4886248
OpenAlexW2300811987

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.