ReviewCell cycle (Georgetown, Tex.)2022
Cell senescence, rapamycin and hyperfunction theory of aging.
Review in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05535608 (The Impact of a Natural Ingredients and App Based Intervention Targeting the Nine Hallmarks of Aging on DNA Methylation), which is not on this map. Cited by 49 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.
The Impact of a Natural Ingredients and App Based Intervention Targeting the Nine Hallmarks of Aging on DNA Methylation
Who cites it
49 citing papers in PubMed, 57 citations in OpenAlex.
- The Zinc-Senescence Axis in Skin Aging and Wound Healing: A Narrative Review.International journal of molecular sciences · 2026Review
- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Chemical Profiles of the Ethanol Extract of Coreopsis Tinctoria Nutt. Based on UHPLC-LTQ-Orbitrap-MS/MS and MSACS omega · 2026Article
- In silico screening, synthesis, and biological evaluation of pyrazolopyrimidine-derived mTOR inhibitors for anticancer and senomorphic effects.Cancer cell international · 2026Article
- Old worms, new tricks: dynamical instability explains late-life rejuvenation inbioRxiv : the preprint server for biology · 2026Article
- Glycative Stress Disrupts the Mitochondrial-Lysosome Axis and Promotes Geroconversion in Aging Cardiomyocytes.Aging cell · 2026Article
- Epigenetic program of ontogenesis and hyperfunction theory: reinterpreting the mechanisms of aging.Frontiers in aging · 2026Article
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- Rapamycin improves endometriosis‑related infertility involving ovarian senescence via the PPARα/IGFBP2 pathway.Molecular medicine reports · 2026Article
- Corticotropin-releasing hormone inhibits autophagy by suppressing PTEN to promote apoptosis in dermal papilla cells.Annals of medicine · 2025Article
- Aging Reduces Intestinal Stem Cell Activity in Killifish and Intermittent Fasting Reverses Intestinal Gene Expression Patterns.Aging cell · 2025Article
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Empagliflozin slows down natural kidney senescence via Six1/Wnt4/NF-κB pathway.Biogerontology · 2025Article
- Evidence for an energetic trade-off model linking inflammaging and immunosenescence in the US Health and Retirement Study and UK Biobank.bioRxiv : the preprint server for biology · 2025Article
- ATF3 Deficiency Exacerbates Ageing-Induced Atherosclerosis and Clinical Intervention Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Enlarged PML-nuclear bodies trigger conflicting cell cycle signal-mediated cytotoxicity in leukemia cells.Cell death & disease · 2025Article
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- PD-1-Enhanced Treg Cell Senescence in Advanced Maternal Age.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-Cell Analysis Dissects the Effects of Vitamin D on Genetic Senescence Signatures Across Murine Tissues.Nutrients · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of cellular senescence is proliferation-like activity of growth-promoting pathways (such as mTOR and MAPK) in non-proliferating cells. When the cell cycle is arrested, these pathways convert arrest to senescence (geroconversion), rendering cells hypertrophic, beta-Gal-positive and hyperfunctional. The senescence-associated secretory phenotype (SASP) is one of the numerous hyperfunctions. Figuratively, geroconversion is a continuation of growth in non-proliferating cells. Rapamycin, a reversible inhibitor of growth, slows down mTOR-driven geroconversion. Developed two decades ago, this model had accurately predicted that rapamycin must extend life span of animals. However, the notion that senescent cells directly cause organismal aging is oversimplified. Senescent cells contribute to organismal aging but are not strictly required. Cell senescence and organismal aging can be linked indirectly via the same underlying cause, namely hyperfunctional signaling pathways such as mTOR.
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What 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.