Evidence map›Paper›PMID 28878685›Full record

ReviewFrontiers in physiology2017

Oxidative Stress-Mediated Atherosclerosis: Mechanisms and Therapies.

Xinyu Yang, Yang Li, Yanda Li, Xiaomeng Ren, Xiaoyu Zhang, Dan Hu, Yonghong Gao, Yanwei Xing, Hongcai Shang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed, 3 pooled it
14.9field-weighted citation impact, top 1% 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

203 citing papers in PubMed, 3 syntheses or guidelines pooled it, 396 citations in OpenAlex.

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  12. Unlocking Novel Therapeutic Potential of Angiotensin II Receptor Blockers.International journal of molecular sciences · 2025
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143 more citing papers are in PubMed but not listed here.

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

9 authors at 5 institutions in 2 countries.

Xinyu YangGuang'anmen Hospital, Chinese Academy of Chinese Medical SciencesBeijing, China.
Yang LiDepartment of Cardiology, General Hospital of People's Liberation ArmyBeijing, China.
Yanda LiGuang'anmen Hospital, Chinese Academy of Chinese Medical SciencesBeijing, China.
Xiaomeng RenGuang'anmen Hospital, Chinese Academy of Chinese Medical SciencesBeijing, China.
Xiaoyu ZhangKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese MedicineBeijing, China.
Dan HuMasonic Medical Research LaboratoryUtica, NY, United States.
Yonghong GaoKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese MedicineBeijing, China.
Yanwei XingGuang'anmen Hospital, Chinese Academy of Chinese Medical SciencesBeijing, China.
Hongcai ShangKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese MedicineBeijing, China.
Beijing University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNGuang’anmen Hospital · CNMasonic Medical Research Laboratory · USPeople's Liberation Army No. 150 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherogenesis, the formation of atherosclerotic plaques, is a complex process that involves several mechanisms, including endothelial dysfunction, neovascularization, vascular proliferation, apoptosis, matrix degradation, inflammation, and thrombosis. The pathogenesis and progression of atherosclerosis are explained differently by different scholars. One of the most common theories is the destruction of well-balanced homeostatic mechanisms, which incurs the oxidative stress. And oxidative stress is widely regarded as the redox status realized when an imbalance exists between antioxidant capability and activity species including reactive oxygen (ROS), nitrogen (RNS) and halogen species, non-radical as well as free radical species. This occurrence results in cell injury due to direct oxidation of cellular protein, lipid, and DNA or via cell death signaling pathways responsible for accelerating atherogenesis. This paper discusses inflammation, mitochondria, autophagy, apoptosis, and epigenetics as they induce oxidative stress in atherosclerosis, as well as various treatments for antioxidative stress that may prevent atherosclerosis.

Indexed as

apoptosisatherosclerosisautophagyepigeneticsinflammationmitochondriaoxidative stresstherapies

Identifiers

PMID28878685
PMCPMC5572357
OpenAlexW2745418757

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.