Evidence map›Paper›PMID 34307357›Full record

ReviewFrontiers in cell and developmental biology2021

Novel Insights and Current Evidence for Mechanisms of Atherosclerosis: Mitochondrial Dynamics as a Potential Therapeutic Target.

Dan Li, Shengjie Yang, Yanwei Xing, Limin Pan, Ran Zhao, Yixi Zhao, Longtao Liu, Min Wu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

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  14. Target and Cell Therapy for Atherosclerosis and CVD.International journal of molecular sciences · 2023
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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.

Dan LiGuang'an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Shengjie YangGuang'an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Yanwei XingGuang'an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Limin PanGuang'an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Ran ZhaoGuang'an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Yixi ZhaoGuang'an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Longtao LiuXiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Min WuGuang'an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNGuang’anmen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) is the main cause of death worldwide. Atherosclerosis is the underlying pathological basis of CVD. Mitochondrial homeostasis is maintained through the dynamic processes of fusion and fission. Mitochondria are involved in many cellular processes, such as steroid biosynthesis, calcium homeostasis, immune cell activation, redox signaling, apoptosis, and inflammation, among others. Under stress conditions, mitochondrial dynamics, mitochondrial cristae remodeling, and mitochondrial ROS (mitoROS) production increase, mitochondrial membrane potential (MMP) decreases, calcium homeostasis is imbalanced, and mitochondrial permeability transition pore open (mPTP) and release of mitochondrial DNA (mtDNA) are activated. mtDNA recognized by TLR9 can lead to NF-κB pathway activation and pro-inflammatory factor expression. At the same time, TLR9 can also activate NLRP3 inflammasomes and release interleukin, an event that eventually leads to tissue damage and inflammatory responses. In addition, mitochondrial dysfunction may amplify the activation of NLRP3 through the production of mitochondrial ROS, which together aggravate accumulating mitochondrial damage. In addition, mtDNA defects or gene mutation can lead to mitochondrial oxidative stress. Finally, obesity, diabetes, hypertension and aging are risk factors for the progression of CVD, which are closely related to mitochondrial dynamics. Mitochondrial dynamics may represent a new target in the treatment of atherosclerosis. Antioxidants, mitochondrial inhibitors, and various new therapies to correct mitochondrial dysfunction represent a few directions for future research on therapeutic intervention and amelioration of atherosclerosis.

Indexed as

cytoskeletonfissionfusionmitochondriamorphologytransport

Identifiers

PMID34307357
PMCPMC8293691
OpenAlexW3178760448

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.