Evidence map›Paper›PMID 35303170›Full record

ReviewAngiogenesis2022

Molecular mechanisms of coronary microvascular endothelial dysfunction in diabetes mellitus: focus on mitochondrial quality surveillance.

Danan Sun, Jin Wang, Sam Toan, David Muid, Ruibing Li, Xing Chang, Hao Zhou

Abstract readReview
PubMed Publisher
In one paragraph

Review in Angiogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
10.6field-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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

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8 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

7 authors at 6 institutions in 2 countries.

Danan SunThe Second Affiliated Hospital of Heilongjiang, University of Chinese Medicine, Harbin, 150001, China.
Jin WangDepartment of Vascular Medicine, Peking University Shougang Hospital, Beijing, 100144, China.
Sam ToanDepartment of Chemical Engineering, University of Minnesota-Duluth, Duluth, MN, 55812, USA.
David MuidPerelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Ruibing LiSenior Department of Cardiology, The Sixth Medical Center of People's Liberation Army General Hospital, Beijing, China.
Xing ChangGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China. xingchang_tcm@outlook.com.
Hao ZhouSenior Department of Cardiology, The Sixth Medical Center of People's Liberation Army General Hospital, Beijing, China. zhouhao@plagh.org.ORCID 0000-0001-8138-7275
Chinese Academy of Medical Sciences & Peking Union Medical College · CNHeilongjiang University of Chinese Medicine · CNPeking University Shougang Hospital · CNUniversity of Minnesota, Duluth · USUniversity of Pennsylvania · USUniversity of Wyoming · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary microvascular endothelial dysfunction is both a culprit and a victim of diabetes, and can accelerate diabetes-related microvascular and macrovascular complications by promoting vasoconstrictive, pro-inflammatory and pro-thrombotic responses. Perturbed mitochondrial function induces oxidative stress, disrupts metabolism and activates apoptosis in endothelial cells, thus exacerbating the progression of coronary microvascular complications in diabetes. The mitochondrial quality surveillance (MQS) system responds to stress by altering mitochondrial metabolism, dynamics (fission and fusion), mitophagy and biogenesis. Dysfunctional mitochondria are prone to fission, which generates two distinct types of mitochondria: one with a normal and the other with a depolarized mitochondrial membrane potential. Mitochondrial fusion and mitophagy can restore the membrane potential and homeostasis of defective mitochondrial fragments. Mitophagy-induced decreases in the mitochondrial population can be reversed by mitochondrial biogenesis. MQS abnormalities induce pathological mitochondrial fission, delayed mitophagy, impaired metabolism and defective biogenesis, thus promoting the accumulation of unhealthy mitochondria and the activation of mitochondria-dependent apoptosis. In this review, we examine the effects of MQS on mitochondrial fitness and explore the association of MQS disorders with coronary microvascular endothelial dysfunction in diabetes. We also discuss the potential to treat diabetes-related coronary microvascular endothelial dysfunction using novel MQS-altering drugs.

Indexed as

Diabetes MellitusEndothelial CellsHumansMitochondriaMitochondrial DynamicsMitophagyBiogenesisCoronary microvascular endothelial dysfunctionDiabetesMitochondrial dynamicsMitochondrial metabolismMitochondrial quality surveillanceMitophagy

Identifiers

PMID35303170
OpenAlexW4221083268

What OpenQuestion holds

Textmetadata
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.