ReviewBiogerontology2025
CHIP and aging: a key regulator of proteostasis and cellular senescence.
Review in Biogerontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed.
- Natural longevity modulator: aging modulatory effects of Eurycoma longifolia Jack polysaccharides in C. elegans and D. melanogaster.Biogerontology · 2026Article
- A prospective study on the regulation of osteoarthritis risk through inflammatory pathways in clonal hematopoiesis.GeroScience · 2026Article
- Physiological responses to mask-associated COFrontiers in public health · 2026Review
- Increasing Life Expectancy with Plant Polyphenols: Lessons from the Mediterranean and Japanese Diets.Molecules (Basel, Switzerland) · 2025Review
- Aging Effects on Absolute and Relative Estrogen Receptor Variant Gene Expression Levels in Male Versus Female Rat Ventromedial Hypothalamic Nucleus Growth Hormone-Releasing Hormone Neurons.Journal of integrative neuroscience · 2025Article
- Investigating Potential Biomarkers of Ankylosing Spondylitis: A Study on Mitochondrial and Senescence Pathways Using Machine Learning.Journal of inflammation research · 2025Article
- Heat shock proteins in atrial fibrillation: from bench to bedside.Frontiers in physiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Degradation of proteostasis, mitochondrial function, and cellular stress resistance results in a build-up of damaged proteins, oxidative insult, and chronic inflammation, characteristic of aging. CHIP is essential for maintaining protein quality control and cellular homeostasis by having dual E3 ubiquitin ligase and co-chaperone activities. CHIP facilitates proteostasis by maintaining proteostasis in misfolded, aggregated proteins by promoting their degradation. Mitochondrial dysfunction, oxidative imbalance, and cellular senescence are caused by its age-associated decline and contribute to neurodegenerative, cardiovascular, and oncogenic disease pathogenesis. Examples of recent pharmacological and gene-based strategies to correct CHIP and restore stress resilience have been made. This review examines the multiple facets of the aging role of CHIP and its potential as an aging disease therapy target.
Indexed as
Identifiers
40323531What OpenQuestion holds
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.