Evidence mapPaperPMID 36834896Full record

ReviewInternational journal of molecular sciences2023

Mitochondrial Homeostasis in VSMCs as a Central Hub in Vascular Remodeling.

Yi Xia, Xu Zhang, Peng An, Junjie Luo, Yongting Luo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
8.9field-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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. ZHX2 Alleviates Vascular Remodeling and Smooth Muscle Cell Proliferation by Transcriptional Regulation of GADD45G.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  12. Nanomaterial-induced mitochondrial biogenesis enhances intercellular mitochondrial transfer efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
  14. How to measure and model cardiovascular aging.Cardiovascular research · 2025
    Review
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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

5 authors at 1 institution in 1 country.

Yi XiaDepartment of Nutrition and Health, China Agricultural University, Beijing 100193, China.
Xu ZhangDepartment of Nutrition and Health, China Agricultural University, Beijing 100193, China.ORCID 0000-0002-3274-3787
Peng AnDepartment of Nutrition and Health, China Agricultural University, Beijing 100193, China.ORCID 0000-0002-0421-0035
Junjie LuoDepartment of Nutrition and Health, China Agricultural University, Beijing 100193, China.ORCID 0000-0002-8987-0533
Yongting LuoDepartment of Nutrition and Health, China Agricultural University, Beijing 100193, China.ORCID 0000-0001-7834-8742
China Agricultural University · CN

Funding

Beijing Municipal Natural Science Foundation 7222111Chinese Universities Scientific Fund 2020TC015National Natural Science Foundation of China 31970717, 82170429
6 · The paper itself

Abstract

Vascular remodeling is a common pathological hallmark of many cardiovascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant cell type lining the tunica media and play a crucial role in maintaining aortic morphology, integrity, contraction and elasticity. Their abnormal proliferation, migration, apoptosis and other activities are tightly associated with a spectrum of structural and functional alterations in blood vessels. Emerging evidence suggests that mitochondria, the energy center of VSMCs, participate in vascular remodeling through multiple mechanisms. For example, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α)-mediated mitochondrial biogenesis prevents VSMCs from proliferation and senescence. The imbalance between mitochondrial fusion and fission controls the abnormal proliferation, migration and phenotypic transformation of VSMCs. Guanosine triphosphate-hydrolyzing enzymes, including mitofusin 1 (MFN1), mitofusin 2 (MFN2), optic atrophy protein 1 (OPA1) and dynamin-related protein 1 (DRP1), are crucial for mitochondrial fusion and fission. In addition, abnormal mitophagy accelerates the senescence and apoptosis of VSMCs. PINK/Parkin and NIX/BINP3 pathways alleviate vascular remodeling by awakening mitophagy in VSMCs. Mitochondrial DNA (mtDNA) damage destroys the respiratory chain of VSMCs, resulting in excessive ROS production and decreased ATP levels, which are related to the proliferation, migration and apoptosis of VSMCs. Thus, maintaining mitochondrial homeostasis in VSMCs is a possible way to relieve pathologic vascular remodeling. This review aims to provide an overview of the role of mitochondria homeostasis in VSMCs during vascular remodeling and potential mitochondria-targeted therapies.

Indexed as

Muscle, Smooth, VascularVascular RemodelingDNA, MitochondrialHomeostasisHumansMitochondriaMitochondrial DynamicsDNA, MitochondrialfissionfusionmitochondriamitophagymtDNAvascular remodelingVSMC

Identifiers

PMID36834896
PMCPMC9961025
OpenAlexW4319983263

What Socratic 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 Socratic graph.