Evidence mapPaperPMID 40538812Full record

ReviewFrontiers in endocrinology2025

Endoplasmic reticulum-mitochondria crosstalk: new mechanisms in the development of atherosclerosis.

Mingxiao Li, Yili Xiao, Ling Dai, Simin Chen, Wanjuan Pei, Chao Tan

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
field-weighted citation impact
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

11 citing papers in PubMed.

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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

6 authors.

Mingxiao Li *Medical School, Hunan University of Chinese Medicine, Changsha, China.
Yili Xiao *Medical School, Hunan University of Chinese Medicine, Changsha, China.
Ling DaiMedical School, Hunan University of Chinese Medicine, Changsha, China.
Simin ChenMedical School, Hunan University of Chinese Medicine, Changsha, China.
Wanjuan PeiMedical School, Hunan University of Chinese Medicine, Changsha, China.
Chao TanDepartment of Cardiology, The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis (AS) is a global public health concern and involves a complex pathogenesis characterized by lipid abnormalities, oxidative stress, and inflammatory responses at the cellular and molecular levels. The crosstalk between the endoplasmic reticulum (ER) and mitochondria, mediated by mitochondria-associated membranes (MAMs), plays a critical role in the pathogenesis of atherosclerosis. As two key cellular organelles, the ER and mitochondria interact physically and functionally through MAMs, which serve as bridges between their close contact and interdependence. MAMs maintain lipid homeostasis, promote calcium ion transport, the oxidative stress response, apoptosis, and autophagy. Recent studies have highlighted the significance of ER-mitochondria crosstalk in the progression of AS, as indicated by mitochondrial and ER structural and functional integrity, redox homeostasis, and calcium homeostasis. This review comprehensively explores the novel mechanisms of ER-mitochondria crosstalk in AS and emphasizes the potential of MAMs as therapeutic targets, aiming to provide new perspectives and strategies for the treatment of cardiovascular diseases.

Indexed as

AtherosclerosisEndoplasmic ReticulumMitochondriaAnimalsHumansOxidative Stressatherosclerosisendoplasmic reticulumendoplasmic reticulum contact complexendoplasmic reticulum-mitochondrial crosstalkmitochondriamitochondria-associated membranes (MAMs)

Identifiers

PMID40538812
PMCPMC12176567

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.