Evidence map›Paper›PMID 38434290›Full record

ArticleHeliyon2024

eIF2α-mediated integrated stress response links multiple intracellular signaling pathways to reprogram vascular smooth muscle cell fate in carotid artery plaque.

Jichang Luo, Xiao Zhang, Wenjing Li, Tao Wang, Shengyan Cui, Tianhua Li, Yilin Wang, Wenlong Xu, Yan Ma, Bin Yang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Hydrogen Sulfide (HAntioxidants (Basel, Switzerland) · 2025
    Article
  2. International journal of molecular sciences · 2025
    Review
  3. Review
  4. Review
  5. Article
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

14 authors at 2 institutions in 1 country.

Jichang LuoDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Xiao ZhangDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Wenjing LiLaboratory of Computational Biology and Machine Intelligence, National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, Beijing, China.
Tao WangDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Shengyan CuiDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Tianhua LiDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Yilin WangInstitute of Cerebrovascular Disease Research and Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China.
Wenlong XuDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Yan MaDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Bin YangDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Yumin LuoInstitute of Cerebrovascular Disease Research and Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China.
Ge YangLaboratory of Computational Biology and Machine Intelligence, National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, Beijing, China.
Ran XuDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Liqun JiaoDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Capital Medical University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Carotid arterial atherosclerotic stenosis is a well-recognized pathological basis of ischemic stroke; however, its underlying molecular mechanisms remain unknown. Vascular smooth muscle cells (VSMCs) play fundamental roles in the initiation and progression of atherosclerosis. Organelle dynamics have been reported to affect atherosclerosis development. However, the association between organelle dynamics and various cellular stresses in atherosclerotic progression remain ambiguous. Methods: In this study, we conducted transcriptomics and bioinformatics analyses of stable and vulnerable carotid plaques. Primary VSMCs were isolated from carotid plaques and subjected to histopathological staining to determine their expression profiles. Endoplasmic reticulum (ER), mitochondria, and lysosome dynamics were observed in primary VSMCs and VSMC cell lines using live-cell imaging. Moreover, the mechanisms underlying disordered organelle dynamics were investigated using comprehensive biological approaches. Results: ER whorls, a representative structural change under ER stress, are prominent dynamic reconstructions of VSMCs between vulnerable and stable plaques, followed by fragmented mitochondria and enlarged lysosomes, suggesting mitochondrial stress and lysosomal defects, respectively. Induction of mitochondrial stress alleviated ER stress and autophagy in an eukaryotic translation initiation factor (eIF)-2α-dependent manner. Furthermore, the effects of eIF2α on ER stress, mitochondrial stress, and lysosomal defects were validated using clinical samples. Conclusion: Our results indicate that morphological and functional changes in VSMC organelles, especially in ER whorls, can be used as reliable biomarkers for atherosclerotic progression. Moreover, eIF2α plays an important role in integrating multiple stress-signaling pathways to determine the behavior and fate of VSMCs.

Indexed as

Carotid artery atherosclerosisOrganellesPlaque vulnerabilityPrimary vascular smooth muscle cellsTranslation initiation factor 2α

Identifiers

PMID38434290
PMCPMC10907769
OpenAlexW4392103378

What OpenQuestion holds

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LicenceCC BY-NC
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.