Evidence map›Paper›PMID 37736860›Full record

ArticleCell stress & chaperones2023

RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress.

Ziwei Zhu, Jie Pu, Yongnan Li, Jianshu Chen, Hong Ding, Anyu Zhou, XiaoWei Zhang

Open access · greenAbstract read
In one paragraph

Article in Cell stress & chaperones, 2023. 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
3.1field-weighted citation impact, top 8% 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, 15 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

7 authors at 3 institutions in 2 countries.

Ziwei ZhuDepartment of Cardiovascular Medicine, Lanzhou University Second Hospital, Lanzhou, 730000, China.
Jie PuDepartment of Cardiovascular Medicine, Lanzhou University Second Hospital, Lanzhou, 730000, China.
Yongnan LiDepartment of Cardiac Surgery, Lanzhou University Second Hospital, Lanzhou, 730000, China.
Jianshu ChenDepartment of Cardiovascular Medicine, Lanzhou University Second Hospital, Lanzhou, 730000, China.
Hong DingDepartment of Cardiovascular Medicine, Lanzhou University Second Hospital, Lanzhou, 730000, China.
Anyu ZhouDepartment of Cardiology, Warren Alpert School of Medicine at Brown University, Providence, RI, USA.
XiaoWei ZhangDepartment of Cardiovascular Medicine, Lanzhou University Second Hospital, Lanzhou, 730000, China. xwzhang@lzu.edu.cn.
Lanzhou University Second Hospital · CNLanzhou University · CNBrown University · US

Funding

Cuiying Scientific and Technological Innovation Program of Lanzhou University Second Hospital CY2019-MS15Gansu heart rehabilitation engineering research center CRQI-C00535Gansu Provincial Department of education project 2020B-024National Natural Science Foundation of China No. NSFC,82060080Project of Lanzhou science and Technology Bureau 2019-RC36Science and Technology Program of Gansu Province 20YF3WA016
6 · The paper itself

Abstract

Ischemic heart failure (HF) is one of the leading causes of global morbidity and mortality; blocking the apoptotic cascade could help improve adverse outcomes of it. RNA-binding motif protein 25 (RBM25) is an RNA-binding protein related to apoptosis; however, its role remains unknown in ischemic HF. The main purpose of this study is to explore the mechanism of RBM25 in ischemic HF. Establishing an ischemic HF model and oxygen-glucose deprivation (OGD) model. ELISA was performed to evaluate the BNP level in the ischemic HF model. Echocardiography and histological analysis were performed to assess cardiac function and infarct size. Proteins were quantitatively and locationally analyzed by western blotting and immunofluorescence. The morphological changes of endoplasmic reticulum (ER) were observed with ER-tracker. Cardiac function and myocardial injury were observed in ischemic HF rats. RBM25 was elevated in cardiomyocytes of hypoxia injury hearts and localized in nucleus both in vitro and in vivo. In addition, cell apoptosis was significantly increased when overexpressed RBM25. Moreover, ER stress stimulated upregulation of RBM25 and promoted cell apoptosis through the CHOP related pathway. Finally, inhibiting the expression of RBM25 could ameliorate the apoptosis and improve cardiac function through blocking the activation of CHOP signaling pathway. RBM25 is significantly upregulated in ischemic HF rat heart and OGD model, which leads to apoptosis by modulating the ER stress through CHOP pathway. Knockdown of RBM25 could reverse apoptosis-mediated cardiac dysfunction. RBM25 may be a promising target for the treatment of ischemic HF.

Indexed as

HypoxiaMyocytes, CardiacAnimalsApoptosisCell LineEndoplasmic Reticulum StressOxygenRatsOxygenApoptosisEndoplasmic reticulum stressIschemic heart failureMyocardial infarctionRBM25

Identifiers

PMID37736860
PMCPMC10746693
OpenAlexW4386945498

What OpenQuestion holds

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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.