LINP1 and radiation-induced senescence in keratinocytes and skin explants
In this abstract, the long non-coding RNA LINP1 rose after ionizing radiation and reduced radiation-induced senescence in keratinocytes via the mTOR-p53 axis; in human skin explants, removing LINP1 worsened radiation damage and senescence features. [1]
Automatic summary · not editorially reviewed
The key findings
LINP1, a long non-coding RNA, was markedly upregulated after ionizing radiation, and functional assays indicated it promoted cell survival and limited radiation-induced DNA damage accumulation. [1]
LINP1 attenuated radiation-induced senescence via the mTOR-p53 axis, binding mTOR's FAT domain and reducing p53 Ser15 phosphorylation; in human skin explants, LINP1 depletion worsened damage and senescence phenotypes. [1]
The authors describe LINP1 as a radioprotective long non-coding RNA and a conceptual basis for future RNA-based radioprotective strategies, not an existing therapy. [1]
The source at a glance
- Study type / format
- Preclinical laboratory study (abstract)
- Population / context
- Keratinocytes and ex vivo human skin explants in laboratory experiments
- Summary based on
- Study abstract
- Original publication
- August 13, 2026
LINP1 rise after radiation in keratinocytes
The abstract reports that LINP1, a long non-coding RNA, was markedly upregulated after ionizing radiation. Functional assays indicated that LINP1 promoted cell survival and limited the accumulation of radiation-induced DNA damage. The authors frame radiation-induced skin injury as a clinical problem in radiotherapy and cellular senescence as a driver of its pathogenesis. These are cell-based assay results described in the abstract, not evidence of benefit in patients.
Supporting source [1]
mTOR-p53 axis and human skin explants
Mechanistically, the abstract states that LINP1 attenuates radiation-induced cellular senescence through the mTOR-p53 signaling axis. LINP1 is said to bind the FAT domain of mTOR via a central nucleotide region called the mTOR-binding domain, weakening the interaction between mTOR and p53; this reduced p53 phosphorylation at Ser15 and downstream senescence-associated signaling. In ex vivo human skin explants, depleting LINP1 worsened radiation-induced tissue damage, persistent DNA damage accumulation and senescence-associated phenotypes. Ex vivo explants are tissue kept outside the body, not a clinical trial.
Supporting source [1]
Abstract-only scope and proposed RNA strategy
The authors conclude that LINP1 is a radioprotective long non-coding RNA regulating radiation-induced senescence through the mTOR-p53 axis. They present this as a conceptual basis for future development of RNA-based radioprotective strategies, not as an existing or approved therapy. The abstract does not report patient numbers, study design details, follow-up or human clinical outcomes. The full text was not reviewed, so methods and statistics cannot be checked here.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Patient numbers, study design, follow-up and human clinical outcomes are not reported. Cell assays and ex vivo skin explants do not establish clinical benefit, and the RNA strategy is proposed, not validated.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Liang X, Hou M, Liu Y, Yang Y, Zhang C, Zhang Z, Zhou L. · europepmc.org · August 13, 2026