Evidence map›Paper›PMID 38250662›Full record

ReviewFrontiers in physiology2023

Mitochondrial-related microRNAs and their roles in cellular senescence.

Ling Luo, Xingna An, Yinghui Xiao, Xiguang Sun, Sijie Li, Yingzhao Wang, Weixia Sun, Dehai Yu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  10. Mitochondrial medicine in obesity: a scoping review.Open medicine (Warsaw, Poland) · 2026
    Review
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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

8 authors at 2 institutions in 1 country.

Ling LuoPublic Research Platform, The First Hospital of Jilin University, Changchun, Jilin, China.
Xingna AnPublic Research Platform, The First Hospital of Jilin University, Changchun, Jilin, China.
Yinghui XiaoPublic Research Platform, The First Hospital of Jilin University, Changchun, Jilin, China.
Xiguang SunDepartment of Hand Surgery, The First Hospital of Jilin University, Changchun, Jilin, China.
Sijie LiDepartment of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China.
Yingzhao WangDepartment of Neurology, Qianwei Hospital of Jilin Province, Changchun, Jilin, China.
Weixia SunDepartment of Nephrology, The First Hospital of Jilin University, Changchun, Jilin, China.
Dehai YuPublic Research Platform, The First Hospital of Jilin University, Changchun, Jilin, China.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a natural aspect of mammalian life. Although cellular mortality is inevitable, various diseases can hasten the aging process, resulting in abnormal or premature senescence. As cells age, they experience distinctive morphological and biochemical shifts, compromising their functions. Research has illuminated that cellular senescence coincides with significant alterations in the microRNA (miRNA) expression profile. Notably, a subset of aging-associated miRNAs, originally encoded by nuclear DNA, relocate to mitochondria, manifesting a mitochondria-specific presence. Additionally, mitochondria themselves house miRNAs encoded by mitochondrial DNA (mtDNA). These mitochondria-residing miRNAs, collectively referred to as mitochondrial miRNAs (mitomiRs), have been shown to influence mtDNA transcription and protein synthesis, thereby impacting mitochondrial functionality and cellular behavior. Recent studies suggest that mitomiRs serve as critical sensors for cellular senescence, exerting control over mitochondrial homeostasis and influencing metabolic reprogramming, redox equilibrium, apoptosis, mitophagy, and calcium homeostasis-all processes intimately connected to senescence. This review synthesizes current findings on mitomiRs, their mitochondrial targets, and functions, while also exploring their involvement in cellular aging. Our goal is to shed light on the potential molecular mechanisms by which mitomiRs contribute to the aging process.

Indexed as

cellular senescenceepigeneticsmitochondriamitomiRsnoncoding RNA

Identifiers

PMID38250662
PMCPMC10796628
OpenAlexW4390611360

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.