Evidence map›Paper›PMID 33611830›Full record

ArticleJournal of cellular and molecular medicine2021

MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway.

Wenhua Lei, Junli Li, Changming Li, Li Chen, Fangyang Huang, Dan Xiao, Jialiang Zhang, Jiahao Zhao, Guoyong Li, Tianyi Qu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 11 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

13 authors at 1 institution in 1 country.

Wenhua LeiDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-5324-3503
Junli LiLaboratory of Cardiovascular Diseases, Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China.
Changming LiDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Li ChenDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Fangyang HuangDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-3049-2996
Dan XiaoDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Jialiang ZhangDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Jiahao ZhaoDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Guoyong LiDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Tianyi QuDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Hao ZhouDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Yanbiao LiaoDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Mao ChenDepartment of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Sichuan University · CN

Funding

National Natural Science Foundation of China 11902211National Natural Science Foundation of China 81600347National Natural Science Foundation of China 81800433National Natural Science Foundation of China 81900258National Natural Science Foundation of China 81900348Sichuan Science and Technology Program 2017SZ0054Sichuan Science and Technology Program 2019YFS0299Sichuan Science and Technology Program 2020YFS0246
6 · The paper itself

Abstract

MARCH5 is a critical regulator of mitochondrial dynamics, apoptosis and mitophagy. However, its role in cardiovascular system remains poorly understood. This study aimed to investigate the role of MARCH5 in endothelial cell (ECs) injury and the involvement of the Akt/eNOS signalling pathway in this process. Rat models of myocardial infarction (MI) and human cardiac microvascular endothelial cells (HCMECs) exposed to hypoxia (1% O

Indexed as

Signal TransductionAnimalsCells, CulturedChromonesEndothelial CellsEndothelium, VascularHumansMaleMembrane ProteinsMorpholinesMyocardial Reperfusion InjuryNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRats2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesMARCHF5 protein, humanMembrane ProteinsMorpholinesNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIProtein Kinase InhibitorsProto-Oncogene Proteins c-aktUbiquitin-Protein Ligasesendothelial cellsendothelial nitric oxide synthaseMARCH5myocardial infarction

Identifiers

PMID33611830
PMCPMC8034466
OpenAlexW3130210078

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.