Evidence map›Paper›PMID 32983930›Full record

ReviewJournal of translational internal medicine2020

The Role of Mitochondria in Vascular Calcification.

Pengbo Wang, Naijin Zhang, Boquan Wu, Shaojun Wu, Ying Zhang, Yingxian Sun

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of translational internal medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  4. PMCell biochemistry and biophysics · 2025
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  19. [Bax inhibitor 1 inhibits vascular calcification in mice by activating optic atrophy 1 expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  20. Review
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

6 authors at 2 institutions in 1 country.

Pengbo WangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Naijin ZhangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Boquan WuDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Shaojun WuDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Ying ZhangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
Yingxian SunDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning Province, China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular calcification (VC) was defined as the ectopic deposition of calcium-phosphorus complexes on the blood vessel walls. It was a process involving multiple factors and mechanisms, covering the phenotype transition of vascular smooth muscle cells (VSMCs) and release of microvesicles. It was a common end-stage alteration of chronic diseases such as cardiovascular disease and chronic kidney disease. Increasing evidence indicates that mitochondria were involved in the development of VC. Mitochondria provided energy to cells, maintained the stability of cell functions, and participated in a variety of biological behavior. Oxidative stress, autophagy, apoptosis, and mitochondrial DNA (mtDNA) damage could affect the development of VSMCs calcification by alteration of mitochondrial function. This article reviewed the mechanism of calcification and the role of mitochondria in VC, aiming to raise a novel insight into drug development and clinical treatment.

Indexed as

apoptosisautophagymitochondriamitochondrial DNAoxidative stressvascular calcification

Identifiers

PMID32983930
PMCPMC7500121
OpenAlexW3043708530

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.