Evidence map›Paper›PMID 31463533›Full record

ArticleBasic research in cardiology2019

Connexin 43 dephosphorylation contributes to arrhythmias and cardiomyocyte apoptosis in ischemia/reperfusion hearts.

Jingyi Xue, Xinxin Yan, Yutong Yang, Min Chen, Lulin Wu, Zhongshan Gou, Zhipeng Sun, Shaletanati Talabieke, Yuanyuan Zheng, Dali Luo

Abstract read
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In one paragraph

Article in Basic research in cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 71 citations in OpenAlex.

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  20. Benefits of SGLT2 inhibitors in arrhythmias.Frontiers in cardiovascular medicine · 2022
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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

10 authors at 1 institution in 1 country.

Jingyi Xue *Department of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Xinxin Yan *Department of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Yutong Yang *Department of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Min ChenDepartment of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Lulin WuDepartment of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Zhongshan GouDepartment of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Zhipeng SunDepartment of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Shaletanati TalabiekeDepartment of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Yuanyuan ZhengDepartment of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China.
Dali LuoDepartment of Pharmacology, Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, School of Basic Medical Sciences, Capital Medical University, District of Fengtai, Street of Youanmenwai, #10 Xitoutiao, Beijing, 100069, People's Republic of China. luodl@ccmu.edu.cn.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Connexin 43 (Cx43)-associated gap junctions form electrical and mechanical conduits between adjacent ventricular cardiomyocytes, ensuring coordinate electrical excitation and synchronic contraction for each heartbeat. Cx43 dephosphorylation is a characteristic of ischemia, arrhythmia, and a failing and aging myocardium, but the exact phosphosite(s) triggering myocardial apoptosis and electrical disturbance and its underlying mechanisms are unclear. We previously found that Cx43-serine 282 phosphorylation (pS282) can regulate cardiomyocyte survival and electrical stability. Here, we investigated the hypothesis that S282 dephosphorylation occurs in and contributes to ischemia/reperfusion (I/R)-induced cardiac injury. We found enhanced Cx43-pS262 and Cx43-pS368 but decreased Cx43-pS282 in rat hearts subjected to I/R (30 min/2 h). I/R rats had ventricular arrhythmias and myocardial apoptosis with activation of the p38 mitogen-activated protein kinase (p38)/factor-associated suicide (Fas)/Fas-associating protein with a novel death domain (FADD) pathway. Similarly, S282 dephosphorylation, abnormal Ca

Indexed as

AnimalsApoptosisArrhythmias, CardiacConnexin 43MaleMyocardial Reperfusion InjuryMyocytes, CardiacPhosphorylationRatsRats, Sprague-DawleySerineConnexin 43Gja1 protein, ratSerineApoptosisArrhythmiaConnexin 43Ischemia/reperfusionPhosphorylation

Identifiers

PMID31463533
OpenAlexW2970080198

What Socratic 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 Socratic graph.