Evidence map›Paper›PMID 27903442›Full record

ReviewAgeing research reviews2017

Are microRNAs true sensors of ageing and cellular senescence?

Justin Williams, Flint Smith, Subodh Kumar, Murali Vijayan, P Hemachandra Reddy

Abstract readReview
In one paragraph

Review in Ageing research reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 96 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Justin WilliamsGarrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
Flint SmithGarrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
Subodh KumarGarrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
Murali VijayanGarrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
P Hemachandra ReddyGarrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Cell Biology & Biochemistry, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neuroscience & Pharmacology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Speech, Language and Hearing Sciences Departments, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Suite E, MS 7495, Lubbock, TX 79413, United States. Electronic address: hemachandra.reddy@ttuhsc.edu.
Institute on Aging · USTexas Tech University Health Sciences Center · US

Funding

Dynamin-Related Protein 1 and Mitochondrial Fragmentation in Alzheimer's DiseaseR01AG042178 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2012 to 2016
$2.0M
Voltage-Dependent Anion Channel and Neurodegeneration in Alzheimer's DiseaseR01AG047812 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2014 to 2018
$1.9M
NIA NIH HHS R01 AG042178NIA NIH HHS R01 AG047812
6 · The paper itself

Abstract

All living beings are programmed to death due to aging and age-related processes. Aging is a normal process of every living species. While all cells are inevitably progressing towards death, many disease processes accelerate the aging process, leading to senescence. Pathologies such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease, cardiovascular disease, cancer, and skin diseases have been associated with deregulated aging. Healthy aging can delay onset of all age-related diseases. Genetics and epigenetics are reported to play large roles in accelerating and/or delaying the onset of age-related diseases. Cellular mechanisms of aging and age-related diseases are not completely understood. However, recent molecular biology discoveries have revealed that microRNAs (miRNAs) are potential sensors of aging and cellular senescence. Due to miRNAs capability to bind to the 3' untranslated region (UTR) of mRNA of specific genes, miRNAs can prevent the translation of specific genes. The purpose of our article is to highlight recent advancements in miRNAs and their involvement in cellular changes in aging and senescence. Our article discusses the current understanding of cellular senescence, its interplay with miRNAs regulation, and how they both contribute to disease processes.

Indexed as

Alzheimer DiseaseMicroRNAsAgingAnimalsCellular SenescenceEpigenesis, GeneticHumansMicroRNAsAgingAlzheimer’s diseasemicroRNAOxidative-stressSenescence

Identifiers

PMID27903442
PMCPMC5357446
OpenAlexW2555863076

What OpenQuestion holds

Textmetadata
LicenceTDM
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.