Evidence map›Paper›PMID 38438604›Full record

ArticleIn vitro cellular & developmental biology. Animal2024

CDC-like kinase 3 deficiency aggravates hypoxia-induced cardiomyocyte apoptosis through AKT signaling pathway.

Xiue Ma, Liming Gao, Rucun Ge, Tianyou Yuan, Bowen Lin, Lixiao Zhen

Abstract read
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Article in In vitro cellular & developmental biology. Animal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

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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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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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

6 authors at 5 institutions in 1 country.

Xiue MaSchool of Medicine, Tongji University, Shanghai, 200092, China.
Liming GaoDepartment of Cardiology, Ji'an Hospital, Shanghai East Hospital, Ji'an, 343000, Jiangxi, China.
Rucun GeShandong Provincial Third Hospital, Shandong University, Jinan, 250012, Shandong, China.
Tianyou YuanDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China. tianyou_yuan@163.com.
Bowen LinSchool of Medicine, Tongji University, Shanghai, 200092, China. bowenlin0512@163.com.
Lixiao ZhenShandong Provincial Third Hospital, Shandong University, Jinan, 250012, Shandong, China. zlxiao56@163.com.
Tongji University · CNShandong Provincial Hospital · CNShandong University · CNShanghai East Hospital · CNShanghai First People's Hospital · CN

Funding

Jiangxi Province Municipal Health Commission Science Technology Grant 202210097Key R&D Program of Shandong Province, China 2019GSF108249Medical and Health Science and Technology Development Program of Shandong Province 202103010947Scientific Research Foundation of Shandong Provincial Third Hospital Q2023001
6 · The paper itself

Abstract

Hypoxia-induced cardiomyocyte apoptosis is one major pathological change of acute myocardial infarction (AMI), but the underlying mechanism remains unexplored. CDC-like kinase 3 (CLK3) plays crucial roles in cell proliferation, migration and invasion, and nucleotide metabolism, however, the role of CLK3 in AMI, especially hypoxia-induced apoptosis, is largely unknown. The expression of CLK3 was elevated in mouse myocardial infarction (MI) models and neonatal rat ventricular myocytes (NRVMs) under hypoxia. Furthermore, CLK3 knockdown significantly promoted apoptosis and inhibited NRVM survival, while CLK3 overexpression promoted NRVM survival and inhibited apoptosis under hypoxic conditions. Mechanistically, CLK3 regulated the phosphorylation status of AKT, a key player in the regulation of apoptosis. Furthermore, overexpression of AKT rescued hypoxia-induced apoptosis in NRVMs caused by CLK3 deficiency. Taken together, CLK3 deficiency promotes hypoxia-induced cardiomyocyte apoptosis through AKT signaling pathway.

Indexed as

ApoptosisCell HypoxiaMyocytes, CardiacProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsMaleMiceMice, Inbred C57BLMyocardial InfarctionPhosphorylationProtein-Tyrosine KinasesRatsRats, Sprague-DawleyClk dual-specificity kinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktAKTCardiomyocyte apoptosisCDC-like kinase 3Hypoxia

Identifiers

PMID38438604
OpenAlexW4392383497

What OpenQuestion holds

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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.