Article in Nature cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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.
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
17 authors.
Rafael Romero-BecerraCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0003-3935-2647
Francisco M CruzCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Alfonso MoraCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0002-6397-4836
Juan Antonio LopezCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Daniela Ponce-BalbuenaCenter for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Andrew AllanCenter for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Roberto Ramos-MondragónCenter for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Bárbara González-TeránCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0002-4336-8644
Marta LeónCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Maria Elena RodríguezCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Luis Leiva-VegaCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Guadalupe Guerrero-SernaCenter for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Eric N Jimenez-VazquezCenter for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
David Filgueiras-RamaCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0001-5909-2454
Jesús VázquezCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0003-1461-5092
José JalifeCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. jose.jalife@cnic.es.ORCID 0000-0003-0080-3500
Guadalupe SabioCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. gsabio@cnic.es.ORCID 0000-0002-2822-0625
Funding
American Heart Association (American Heart Association, Inc.) 14POST17820005American Heart Association (American Heart Association, Inc.) 18POST34080175"la Caixa" Foundation (Caixa Foundation) HR17-00247"la Caixa" Foundation (Caixa Foundation) HR19/52160013Ministerio de Educación, Cultura y Deporte (Ministry of Education, Culture and Sports, Spain) FPU17/03847Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PDC2021-121147-I00Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PGC2018-097019-B-I00Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PID2022-138525OB-I00Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PDC2021-121147-I00Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PMP21/00057U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01 Grant HL122352
6 · The paper itself
Abstract
Ventricular fibrillation (VF) is a leading immediate cause of sudden cardiac death. There is a strong association between aging and VF, although the mechanisms are unclear, limiting the availability of targeted therapeutic interventions. Here we found that the stress kinases p38γ and p38δ are activated in the ventricles of old mice and mice with genetic or drug-induced arrhythmogenic conditions. We discovered that, upon activation, p38γ and p38δ cooperatively increase the susceptibility to stress-induced VF. Mechanistically, our data indicate that activated p38γ and p38δ phosphorylate ryanodine receptor 2 (RyR2) disrupt Kv4.3 channel localization, promoting sarcoplasmic reticulum calcium leak, I
Indexed as
Mitogen-Activated Protein Kinase 12Ryanodine Receptor Calcium Release ChannelVentricular FibrillationAction PotentialsAge FactorsAnimalsCalcium SignalingDisease Models, AnimalEnzyme ActivationHumansMaleMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 13Myocytes, CardiacMitogen-Activated Protein Kinase 12Mitogen-Activated Protein Kinase 13ryanodine receptor 2. mouseRyanodine Receptor Calcium Release Channel
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.
p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia. · full record | OpenQuestion