Evidence map›Paper›PMID 39800969›Full record

ArticleEuropace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology2024

Tumour necrosis factor alpha-induced protein 3-interacting protein 3 overexpression protects against arrhythmogenic remodelling in the heart failure mice.

Hongjie Yang, Xiaoyan Shen, Huibo Wang, Wei Shuai

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Article in Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

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0cells of the map it votes in
6citing papers in PubMed
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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

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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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Concurrent SVT and atrial fibrillation ablation using a dual-energy linear ablation catheter.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Article
  4. Article
  5. Article
  6. Article
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

4 authors.

Hongjie YangDepartment of Cardiology, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuhan 430060, Hubei, P.R. of China.ORCID 0000-0003-0024-9204
Xiaoyan ShenDepartment of Anesthesiology, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuhan 430060, Hubei, P.R. of China.
Huibo WangDepartment of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital; Institute of Cardiovascular Diseases, China Three Gorges University, Hu Bei Clinical Research Center for Ischemic Cardiovascular Disease, No. 183 Yiling Avenue, Yichang 443000, Hubei, China.
Wei ShuaiDepartment of Cardiology, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuhan 430060, Hubei, P.R. of China.ORCID 0000-0002-5507-7369

Funding

Natural Science Foundation of Hubei Province 2023AFB140Open Project of Hubei Key Laboratory 2023KFZZ025
6 · The paper itself

Abstract

aimsVentricular arrhythmias (VAs), which can lead to sudden cardiac death, are the primary cause of mortality in patients with heart failure (HF). However, the precise mechanisms underlying these arrhythmias are not well understood. Recent studies have implicated tumour necrosis factor alpha-induced protein 3-interacting protein 3 (TNIP3) in pathological cardiac hypertrophy. Nevertheless, its role in isoproterenol (ISO)-associated VAs remains elusive. METHODS AND

resultsWe overexpressed TNIP3 in the myocardium using an adeno-associated virus 9 system, administered via tail vein injection. C57BL/6 mice received daily subcutaneous injections of ISO for two consecutive weeks to establish an HF model. We performed histopathology and electrophysiological studies to assess ventricular structural remodelling, electrical remodelling, and susceptibility to VAs. Additionally, RNA sequencing (RNA-Seq) and western blot analysis were conducted to elucidate the underlying mechanisms. The expression of TNIP3 was up-regulated following ISO treatment. TNIP3 overexpression significantly reversed ISO-induced cardiac dysfunction, fibrosis, electrical remodelling, and VAs susceptibility. Accordingly, RNA-Seq identifies that the inflammatory response takes an important role in ISO-induced Vas, and TNIP3 overexpression could alleviate ISO-induced cardiac proinflammatory response by promoting M1 to M2 macrophage polarization. Mechanistically, PI3K/Akt/NF-κB signalling is responsible for the protective effect of TNIP3 overexpression on ISO-induced HF. And PI3K/Akt signalling activation offset the protective effect of TNIP3 overexpression on ISO-induced cardiac inflammation and VAs.

conclusionThe findings of this study highlight the critical role of TNIP3 in ISO-associated cardiac remodelling and VAs, which are induced by the inhibited activation of the PI3K/Akt/NF-κB signalling pathway.

Indexed as

Arrhythmias, CardiacHeart FailureMembrane ProteinsMyocardiumVentricular RemodelingAnimalsDisease Models, AnimalIsoproterenolMaleMiceMice, Inbred C57BLNF-kappa BProto-Oncogene Proteins c-aktSignal TransductionIsoproterenolMembrane ProteinsNF-kappa BProto-Oncogene Proteins c-aktHeart failureInflammationIsoproterenolVentricular arrhythmia

Identifiers

PMID39800969
PMCPMC11757166

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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.