Evidence map›Paper›PMID 38674076›Full record

ReviewInternational journal of molecular sciences2024

Mitochondrial Kinase Signaling for Cardioprotection.

Kerstin Boengler, Chantal Eickelmann, Petra Kleinbongard

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Kerstin BoenglerInstitute of Physiology, Justus-Liebig University, 35392 Giessen, Germany.
Chantal EickelmannInstitute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, 45147 Essen, Germany.ORCID 0000-0002-0508-7593
Petra KleinbongardInstitute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, 45147 Essen, Germany.ORCID 0000-0003-3576-3772
West German Heart and Vascular Center Essen · DEJustus-Liebig-Universität Gießen · DE

Funding

European Union CA22169
6 · The paper itself

Abstract

Myocardial ischemia/reperfusion injury is reduced by cardioprotective adaptations such as local or remote ischemic conditioning. The cardioprotective stimuli activate signaling cascades, which converge on mitochondria and maintain the function of the organelles, which is critical for cell survival. The signaling cascades include not only extracellular molecules that activate sarcolemmal receptor-dependent or -independent protein kinases that signal at the plasma membrane or in the cytosol, but also involve kinases, which are located to or within mitochondria, phosphorylate mitochondrial target proteins, and thereby modify, e.g., respiration, the generation of reactive oxygen species, calcium handling, mitochondrial dynamics, mitophagy, or apoptosis. In the present review, we give a personal and opinionated overview of selected protein kinases, localized to/within myocardial mitochondria, and summarize the available data on their role in myocardial ischemia/reperfusion injury and protection from it. We highlight the regulation of mitochondrial function by these mitochondrial protein kinases.

Indexed as

Mitochondria, HeartMyocardial Reperfusion InjurySignal TransductionAnimalsHumansMitochondriaProtein KinasesReactive Oxygen SpeciesProtein KinasesReactive Oxygen Speciescardioprotectionischemiamitochondriapreconditioningprotein kinasereperfusion

Identifiers

PMID38674076
PMCPMC11049936
OpenAlexW4394953259

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.