ReviewCellular and molecular life sciences : CMLS2007
From old organisms to new molecules: integrative biology and therapeutic targets in accelerated human ageing.
Review in Cellular and molecular life sciences : CMLS, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- The central role of DNA damage in immunosenescence.Frontiers in aging · 2023Review
- Crosstalk Between Senescent Bone Cells and the Bone Tissue Microenvironment Influences Bone Fragility During Chronological Age and in Diabetes.Frontiers in physiology · 2022Review
- Vascular Aging in Rodent Models: Contrasting Mechanisms Driving the Female and Male Vascular Senescence.Frontiers in aging · 2021Review
- Hutchinson-Gilford Progeria Syndrome: A Premature Aging Disease.Molecular neurobiology · 2018Review
- Differential stem cell aging kinetics in Hutchinson-Gilford progeria syndrome and Werner syndrome.Protein & cell · 2018Article
- Physiological and pathological consequences of cellular senescence.Cellular and molecular life sciences : CMLS · 2014Review
- The Drosophila orthologue of progeroid human WRN exonuclease, DmWRNexo, cleaves replication substrates but is inhibited by uracil or abasic sites : analysis of DmWRNexo activity in vitro.Age (Dordrecht, Netherlands) · 2013Article
- Subcellular localization of SREBP1 depends on its interaction with the C-terminal region of wild-type and disease related A-type lamins.Experimental cell research · 2011Article
- Enabling enrichment analysis with the Human Disease Ontology.Journal of biomedical informatics · 2011Article
- Clock genes, hair growth and aging.Aging · 2010Review
- Increasing longevity through caloric restriction or rapamycin feeding in mammals: common mechanisms for common outcomes?Aging cell · 2009Article
- Premature aging.Cellular and molecular life sciences : CMLS · 2009Review
- Roles of RECQ helicases in recombination based DNA repair, genomic stability and aging.Biogerontology · 2009Review
- Accelerated ageing: from mechanism to therapy through animal models.Transgenic research · 2009Review
- Identification and characterization of a Drosophila ortholog of WRN exonuclease that is required to maintain genome integrity.Aging cell · 2008Article
- Cellular senescence and organismal aging.Mechanisms of ageing and developmentReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Understanding the basic biology of human ageing is a key milestone in attempting to ameliorate the deleterious consequences of old age. This is an urgent research priority given the global demographic shift towards an ageing population. Although some molecular pathways that have been proposed to contribute to ageing have been discovered using classical biochemistry and genetics, the complex, polygenic and stochastic nature of ageing is such that the process as a whole is not immediately amenable to biochemical analysis. Thus, attempts have been made to elucidate the causes of monogenic progeroid disorders that recapitulate some, if not all, features of normal ageing in the hope that this may contribute to our understanding of normal human ageing. Two canonical progeroid disorders are Werner's syndrome and Hutchinson-Gilford progeroid syndrome (also known as progeria). Because such disorders are essentially phenocopies of ageing, rather than ageing itself, advances made in understanding their pathogenesis must always be contextualised within theories proposed to help explain how the normal process operates. One such possible ageing mechanism is described by the cell senescence hypothesis of ageing. Here, we discuss this hypothesis and demonstrate that it provides a plausible explanation for many of the ageing phenotypes seen in Werner's syndrome and Hutchinson-Gilford progeriod syndrome. The recent exciting advances made in potential therapies for these two syndromes are also reviewed.
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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.