Evidence map›Paper›PMID 31657084›Full record

ArticleCell proliferation2020

Aconitine induces cardiomyocyte damage by mitigating BNIP3-dependent mitophagy and the TNFα-NLRP3 signalling axis.

Fu Peng, Nan Zhang, Chunting Wang, Xiaoyun Wang, Wei Huang, Cheng Peng, Gu He, Bo Han

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 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

8 authors at 2 institutions in 1 country.

Fu PengWest China School of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Nan ZhangWest China School of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Chunting WangWest China School of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Xiaoyun WangWest China School of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Wei HuangKey Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Cheng PengKey Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Gu HeWest China School of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.ORCID https://orcid.org/0000-0002-1536-8882
Bo HanKey Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.ORCID https://orcid.org/0000-0003-3200-4682
Sichuan University · CNChengdu University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China 21772131National Natural Science Foundation of China 81630101National Natural Science Foundation of China 81773889National Natural Science Foundation of China 81891012Science & Technology Department of Sichuan Province 2017JQ0002Science & Technology Department of Sichuan Province 2017JZYD0001Science & Technology Department of Sichuan Province 2019YFSY0004
6 · The paper itself

Abstract

objectivesAconitine, the natural product extracted from Aconitum species, is widely used for the treatment of various diseases, including rheumatism, arthritis, bruises, fractures and pains. However, many studies have reported cardiotoxicity and neurotoxicity caused by aconitine, but the detailed mechanism underlying aconitine's effect on these processes remains unclear. MATERIALS AND

methodsThe effects of aconitine on the inflammation, apoptosis and viability of H9c2 rat cardiomyocytes were evaluated by flow cytometry, Western blot, RNA sequencing and bioinformatics analysis.

resultsAconitine suppressed cardiomyocyte proliferation and induced inflammation and apoptosis in a dose- and time-dependent manner. These inflammatory damages could be reversed by a TNFα inhibitor and BNIP3-mediated mitophagy. Consistent with the in vitro results, overexpression of BNIP3 in heart tissue partially suppressed the cardiotoxicity of aconitine by inhibiting apoptosis and the NLRP3 inflammasome.

conclusionsOur findings lay a foundation for the application of a TNFα inhibitor and BNIP3 to aconitine-induced cardiac toxicity prevention and therapy, thereby demonstrating potential for further investigation.

Indexed as

AconitineAnimalsCardiotoxicityCell LineMaleMembrane ProteinsMitochondrial ProteinsMitophagyMyocytes, CardiacNLR Family, Pyrin Domain-Containing 3 ProteinRatsRats, Sprague-DawleySignal TransductionTumor Necrosis Factor-alphaAconitineBNIP3 protein, ratMembrane ProteinsMitochondrial ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratTumor Necrosis Factor-alphaaconitineBNIP3cardiomyocytemitophagy

Identifiers

PMID31657084
PMCPMC6985658
OpenAlexW2981902997

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.