ReviewCell death & disease2025
The dual guardians of cellular stability: exploring nesprin and lamin in senescence.
Review in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- miR-182-5p regulates proliferation and senescence in chicken Leydig cells via the Wnt/β-catenin pathway by targeting FOXN3.Poultry science · 2026Article
- Review
- Cellular senescence as a therapeutic target for aging intervention.Biomedical journal · 2026Review
- The role ofFrontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a state where cells permanently exit the cell cycle after a finite number of divisions, while maintaining metabolic activity. This phenomenon, initially described by Leonard Hayflick, plays a pivotal role in aging, contributing to the progressive decline in physiological function by promoting tissue dysfunction and restricting regenerative capacity. It is regulated by an array of factors, including DNA damage, telomere shortening, oxidative stress, mitochondrial dysfunction, and epigenetic modifications. Nesprins, a family of transmembrane proteins embedded in the nuclear envelope, are integral components of the LINC (Linker of Nucleoskeleton and Cytoskeleton) complex, which connects the nucleus to the cytoskeleton, thus preserving structural integrity and facilitating mechanotransduction. Lamin proteins, which form the nuclear lamina beneath the inner nuclear membrane, provide support to nuclear envelope architecture, organize chromatin, and modulate gene expression. Lamin proteins also interact with nesprins to collectively sustain nuclear mechanics and maintain morphological stability. Understanding the molecular mechanisms by which nesprins and lamins influence cellular senescence provides valuable insights into the biology of aging and may offer novel therapeutic avenues to address age-related diseases. This review examines the interactions between nesprin and lamin proteins and their potential contributions to cellular senescence.
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.