Evidence map›Paper›PMID 26685868›Full record

ArticleAging cell2016

Global genome splicing analysis reveals an increased number of alternatively spliced genes with aging.

Sofía A Rodríguez, Diana Grochová, Tomás McKenna, Bhavesh Borate, Niraj S Trivedi, Michael R Erdos, Maria Eriksson

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 101 citations in OpenAlex.

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  17. Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024
    Article
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  19. Inhibition of C5AR1 impairs osteoclast mobilization and prevents bone loss.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 2 countries.

Sofía A RodríguezDepartment of Biosciences and Nutrition, Center for Innovative Medicine, Karolinska Institutet, Novum, SE-141 83, Huddinge, Sweden.
Diana GrochováDepartment of Biosciences and Nutrition, Center for Innovative Medicine, Karolinska Institutet, Novum, SE-141 83, Huddinge, Sweden.
Tomás McKennaDepartment of Biosciences and Nutrition, Center for Innovative Medicine, Karolinska Institutet, Novum, SE-141 83, Huddinge, Sweden.
Bhavesh BorateNational Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Niraj S TrivediNational Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Michael R ErdosNational Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Maria ErikssonDepartment of Biosciences and Nutrition, Center for Innovative Medicine, Karolinska Institutet, Novum, SE-141 83, Huddinge, Sweden.
Karolinska Institutet · SENational Human Genome Research Institute · USNational Institutes of Health · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Alternative splicing (AS) is a key regulatory mechanism for the development of different tissues; however, not much is known about changes to alternative splicing during aging. Splicing events may become more frequent and widespread genome-wide as tissues age and the splicing machinery stringency decreases. Using skin, skeletal muscle, bone, thymus, and white adipose tissue from wild-type C57BL6/J male mice (4 and 18 months old), we examined the effect of age on splicing by AS analysis of the differential exon usage of the genome. The results identified a considerable number of AS genes in skeletal muscle, thymus, bone, and white adipose tissue between the different age groups (ranging from 27 to 246 AS genes corresponding to 0.3-3.2% of the total number of genes analyzed). For skin, skeletal muscle, and bone, we included a later age group (28 months old) that showed that the number of alternatively spliced genes increased with age in all three tissues (P < 0.01). Analysis of alternatively spliced genes across all tissues by gene ontology and pathway analysis identified 158 genes involved in RNA processing. Additional analysis of AS in a mouse model for the premature aging disease Hutchinson-Gilford progeria syndrome was performed. The results show that expression of the mutant protein, progerin, is associated with an impaired developmental splicing. As progerin accumulates, the number of genes with AS increases compared to in wild-type skin. Our results indicate the existence of a mechanism for increased AS during aging in several tissues, emphasizing that AS has a more important role in the aging process than previously known.

Indexed as

AgingAging, PrematureAlternative SplicingAnimalsMaleMiceMice, Inbred C57BLMuscle, SkeletalSkinSkin Physiological Phenomenaagingalternative splicingHGPSNF-κBprogeriaspliceosometranscriptome

Identifiers

PMID26685868
PMCPMC4783335
OpenAlexW2204950746

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.