Evidence map›Paper›PMID 39155403›Full record

ArticleCell proliferation2024

Mechanical stress-induced autophagy is cytoskeleton dependent.

Lin Liu, Wei Zheng, Yuhui Wei, Qian Li, Nan Chen, Qinglin Xia, Lihua Wang, Jun Hu, Xingfei Zhou, Yanhong Sun and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 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
–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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  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

11 authors.

Lin LiuKey Laboratory of Laboratory Medicine, Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.
Wei ZhengShanghai Institute of Applied Physics, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yuhui WeiThe Interdisciplinary Research Center, Shanghai Synchrotron Radiation Facility, Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai, China.
Qian LiFrontiers Science Center for Transformative Molecules and National Center for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China.
Nan ChenSchool of Chemistry and Materials Sciences, Shanghai Normal University, Shanghai, China.ORCID https://orcid.org/0000-0001-8536-6631
Qinglin XiaShanghai Institute of Applied Physics, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Lihua WangInstitute of Materiobiology, College of Science, Shanghai University, Shanghai, China.
Jun HuInstitute of Materiobiology, College of Science, Shanghai University, Shanghai, China.
Xingfei ZhouDepartment of Microelectronic Science and Engineering, School of Physical Science and Technology, Ningbo University, Zhejiang, China.
Yanhong SunInstitute of Materiobiology, College of Science, Shanghai University, Shanghai, China.
Bin LiThe Interdisciplinary Research Center, Shanghai Synchrotron Radiation Facility, Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai, China.

Funding

Foundation of National Facility for Translational Medicine (Shanghai)National Key Research and Development Program of China 2022YFA1603600National Natural Science Foundation of China 12174407Natural Science Foundation of Zhejiang Province LY24H030007
6 · The paper itself

Abstract

The cytoskeleton is essential for mechanical signal transduction and autophagy. However, few studies have directly demonstrated the contribution of the cytoskeleton to mechanical stress-induced autophagy. We explored the role of the cytoskeleton in response to compressive force-induced autophagy in human cell lines. Inhibition and activation of cytoskeletal polymerization using small chemical molecules revealed that cytoskeletal microfilaments are required for changes in the number of autophagosomes, whereas microtubules play an auxiliary role in mechanical stress-induced autophagy. The intrinsic mechanical properties and special intracellular distribution of microfilaments may account for a large proportion of compression-induced autophagy. Our experimental data support that microfilaments are core components of mechanotransduction signals.

Indexed as

AutophagyMechanotransduction, CellularMicrotubulesStress, MechanicalActin CytoskeletonAutophagosomesCell LineCytoskeletonHumans

Identifiers

PMID39155403
PMCPMC11628738

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.