ReviewJournal of molecular medicine (Berlin, Germany)2012
Potential therapeutic approaches for modulating expression and accumulation of defective lamin A in laminopathies and age-related diseases.
Review in Journal of molecular medicine (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Senescence Rejuvenation through Reduction in Mitochondrial Reactive Oxygen Species Generation byAntioxidants (Basel, Switzerland) · 2024Article
- Targeting Mitochondrial Oxidative Stress as a Strategy to Treat Aging and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- The emerging role of cellular senescence in complications of COVID-19.Cancer treatment and research communications · 2021Review
- Sex Differences in Molecular Mechanisms of Cardiovascular Aging.Frontiers in aging · 2021Review
- Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020Review
- Down-Regulation of Lnc-CYP7A1-1 Rejuvenates Aged Human Mesenchymal Stem Cells to Improve Their Efficacy for Heart Repair Through SYNE1.Frontiers in cell and developmental biology · 2020Article
- Molecular therapies delaying cardiovascular aging: disease- or health-oriented approaches.Vascular biology (Bristol, England) · 2020Review
- Suppression of myopathic lamin mutations by muscle-specific activation of AMPK and modulation of downstream signaling.Human molecular genetics · 2019Article
- Are parents of children with Cockayne syndrome manifesting features of the disorder?: Case reports.Medicine · 2017Article
- Chemical screening identifies ROCK as a target for recovering mitochondrial function in Hutchinson-Gilford progeria syndrome.Aging cell · 2017Article
- Aging Chart: a community resource for rapid exploratory pathway analysis of age-related processes.Nucleic acids research · 2016Article
- All-trans retinoic acid and rapamycin normalize Hutchinson Gilford progeria fibroblast phenotype.Oncotarget · 2015Article
- Lamins at the crossroads of mechanosignaling.Genes & development · 2015Review
- Anti-Proliferative Effect of Rosmarinus officinalis L. Extract on Human Melanoma A375 Cells.PloS one · 2015Article
- Longevity expectations in the pension fund, insurance, and employee benefits industries.Psychology research and behavior management · 2015Article
- Signaling pathway cloud regulation for in silico screening and ranking of the potential geroprotective drugs.Frontiers in genetics · 2014Article
- Genetics and epigenetics of aging and longevity.Cell cycle (Georgetown, Tex.) · 2014Review
- Open access integrated therapeutic and diagnostic platforms for personalized cardiovascular medicine.Journal of personalized medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 5 countries.
Funding
Abstract
Scientific understanding of the genetic components of aging has increased in recent years, with several genes being identified as playing roles in the aging process and, potentially, longevity. In particular, genes encoding components of the nuclear lamina in eukaryotes have been increasingly well characterized, owing in part to their clinical significance in age-related diseases. This review focuses on one such gene, which encodes lamin A, a key component of the nuclear lamina. Genetic variation in this gene can give rise to lethal, early-onset diseases known as laminopathies. Here, we analyze the literature and conduct computational analyses of lamin A signaling and intracellular interactions in order to examine potential mechanisms for altering or slowing down aberrant Lamin A expression and/or for restoring the ratio of normal to aberrant lamin A. The ultimate goal of such studies is to ameliorate or combat laminopathies and related diseases of aging, and we provide a discussion of current approaches in this review.
Indexed as
Identifiers
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.