ArticleAging2015
Attenuation of p38α MAPK stress response signaling delays the in vivo aging of skeletal muscle myofibers and progenitor cells.
Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Chronic activation of p38α in skeletal muscle causes necrotic changes, but also abolishes expression of MK2, MK3, and MKK6 and the muscle recovers.The Journal of biological chemistry · 2026Article
- P38α MAPK Coordinates Mitochondrial Adaptation to Caloric Surplus in Skeletal Muscle.International journal of molecular sciences · 2024Article
- Asynchronous Pattern of MAPKs' Activity during Aging of Different Tissues and of Distinct Types of Skeletal Muscle.International journal of molecular sciences · 2024Article
- Age-associated changes in lineage composition of the enteric nervous system regulate gut health and disease.eLife · 2023Article
- Normal and Pathological NRF2 Signalling in the Central Nervous System.Antioxidants (Basel, Switzerland) · 2022Review
- p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?International journal of molecular sciences · 2020Review
- Orienting Muscle Stem Cells for Regeneration in Homeostasis, Aging, and Disease.Cell stem cell · 2018Review
- Aged dominant negative p38α MAPK mice are resistant to age-dependent decline in adult-neurogenesis and context discrimination fear conditioning.Behavioural brain research · 2017Article
- The influence of pro-longevity gene Gclc overexpression on the age-dependent changes in Drosophila transcriptome and biological functions.BMC genomics · 2016Article
- p38 Mitogen activated protein kinase (MAPK): a new therapeutic target for reducing the risk of adverse pregnancy outcomes.Expert opinion on therapeutic targets · 2016Review
- Molecular circuitry of stem cell fate in skeletal muscle regeneration, ageing and disease.Nature reviews. Molecular cell biology · 2016Review
- Schisandrae fructus enhances myogenic differentiation and inhibits atrophy through protein synthesis in human myotubes.International journal of nanomedicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Functional competence and self-renewal of mammalian skeletal muscle myofibers and progenitor cells declines with age. Progression of the muscle aging phenotype involves the decline of juvenile protective factorsi.e., proteins whose beneficial functions translate directly to the quality of life, and self-renewal of progenitor cells. These characteristics occur simultaneously with the age-associated increase of p38α stress response signaling. This suggests that the maintenance of low levels of p38α activity of juvenile tissues may delay or attenuate aging. We used the dominant negative haploinsufficient p38α mouse (DN-p38α(AF/+)) to demonstrate that in vivo attenuation of p38α activity in the gastrocnemius of the aged mutant delays age-associated processes that include: a) the decline of the juvenile protective factors, BubR1, aldehyde dehydrogenase 1A (ALDH1A1), and aldehyde dehydrogenase 2 (ALDH2); b) attenuated expression of p16(Ink4a) and p19(Arf) tumor suppressor genes of the Cdkn2a locus; c) decreased levels of hydroxynonenal protein adducts, expression of COX2 and iNOS; d) decline of the senescent progenitor cell pool level and d) the loss of gastrocnemius muscle mass. We propose that elevated P-p38α activity promotes skeletal muscle aging and that the homeostasis of p38α impacts the maintenance of a beneficial healthspan.
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Registered trials
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.