Evidence map›Paper›PMID 36654782›Full record

ArticleOxidative medicine and cellular longevity2023

Myo1b Promotes Premature Endothelial Senescence and Dysfunction via Suppressing Autophagy: Implications for Vascular Aging.

Yi Yu, Yuanyuan Ren, Zi Li, Yang Li, Yirong Li, Yan Zhang, Runlin Gui, Yue Cui, Lu Qian, Yuyan Xiong

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2023. 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
1.9field-weighted citation impact, top 14% 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, 9 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
  5. Review
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

10 authors at 2 institutions in 1 country.

Yi YuKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0003-1445-1702
Yuanyuan RenKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0002-6059-1127
Zi LiKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0002-1322-1190
Yang LiKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0002-1004-6585
Yirong LiKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0003-1182-1747
Yan ZhangKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0002-4579-4516
Runlin GuiKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0002-5720-5432
Yue CuiKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0002-0578-3740
Lu QianDepartment of Endocrinology, Xi'an No.3 Hospital, The Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0003-2388-0357
Yuyan XiongKey Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences and Medicine, Northwest University, Xi'an, Shaanxi, China.ORCID https://orcid.org/0000-0001-7623-7109
Ministry of Education of the People's Republic of China · CNNorthwest University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cell (EC) senescence characterized by an irreversible growth arrest leading to endothelial dysfunction has been implicated in vascular aging and aging-associated cardiovascular diseases. Autophagy plays a crucial role in the modulation of cellular senescence. Our previous showed that myosin 1b (Myo1b), one family of nonfilamentous class-1 myosin, was reported to be involved in the modulation of human smooth muscle cell senescence. However, the role of Myo1b in the modulation of EC senescence with links to autophagy has yet to be elucidated. In this study, we sought to explore the role of Myo1b in endothelial senescence and further elucidate the underlying mechanisms. Here, we show prominent upregulation of Myo1b in senescent ECs in comparison with nonsenescence ECs in both mRNA and protein expression levels. Silencing Myo1b in senescent cells ameliorates endothelial dysfunctions and reverses endothelial senescence phenotypic changes such as senescence-associated-

Indexed as

AutophagyCellular SenescenceEndothelial CellsAgingAnimalsCalciumHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MiceMyosinsMyosin Type ICalciumLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanLrrk2 protein, mouseMYO1B protein, humanMyo1b protein, mouseMyosinsMyosin Type I

Identifiers

PMID36654782
PMCPMC9842418
OpenAlexW4313855493

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.