Evidence map›Paper›PMID 38858355›Full record

ArticleCell death & disease2024

The miR-30-5p/TIA-1 axis directs cellular senescence by regulating mitochondrial dynamics.

Hyosun Tak, Seongho Cha, Youlim Hong, Myeongwoo Jung, Seungyeon Ryu, Sukyoung Han, Seung Min Jeong, Wook Kim, Eun Kyung Lee

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. 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

9 authors.

Hyosun Tak *Department of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.
Seongho Cha *Department of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.
Youlim HongDepartment of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.
Myeongwoo JungDepartment of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.
Seungyeon RyuDepartment of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.
Sukyoung HanDepartment of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.
Seung Min JeongDepartment of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.ORCID 0000-0002-9787-2539
Wook KimDepartment of Molecular Science & Technology, Ajou University, Suwon, 16499, South Korea.ORCID 0000-0002-7701-4684
Eun Kyung LeeDepartment of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea. leeek@catholic.ac.kr.ORCID 0000-0003-4207-2080

Funding

National Research Foundation of Korea (NRF) 2021R1A2C1004128
6 · The paper itself

Abstract

Senescent cells exhibit a diverse spectrum of changes in their morphology, proliferative capacity, senescence-associated secretory phenotype (SASP) production, and mitochondrial homeostasis. These cells often manifest with elongated mitochondria, a hallmark of cellular senescence. However, the precise regulatory mechanisms orchestrating this phenomenon remain predominantly unexplored. In this study, we provide compelling evidence for decreases in TIA-1, a pivotal regulator of mitochondrial dynamics, in models of both replicative senescence and ionizing radiation (IR)-induced senescence. The downregulation of TIA-1 was determined to trigger mitochondrial elongation and enhance the expression of senescence-associated β-galactosidase, a marker of cellular senescence, in human foreskin fibroblast HS27 cells and human keratinocyte HaCaT cells. Conversely, the overexpression of TIA-1 mitigated IR-induced cellular senescence. Notably, we identified the miR-30-5p family as a novel factor regulating TIA-1 expression. Augmented expression of the miR-30-5p family was responsible for driving mitochondrial elongation and promoting cellular senescence in response to IR. Taken together, our findings underscore the significance of the miR-30-5p/TIA-1 axis in governing mitochondrial dynamics and cellular senescence.

Indexed as

Cellular SenescenceMicroRNAsMitochondriaMitochondrial DynamicsT-Cell Intracellular Antigen-1Cell LineFibroblastsHumansKeratinocytesRadiation, IonizingSignal TransductionMicroRNAsMIRN30b microRNA, humanT-Cell Intracellular Antigen-1TIA1 protein, human

Identifiers

PMID38858355
PMCPMC11164864

What Socratic holds

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Registered trials

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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.