ReviewiScience2026
Cryptic transcription in aging.
Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cryptic transcription is an aberrant form of transcription that initiates from non-canonical, non-promoter regions within the gene. In mammals, a repressive chromatin state effectively inhibits cryptic transcription, preserving transcriptional fidelity. Aging-induced loss of trimethylated lysine 36 on histone H3 reduces DNA methylation, and accumulation of promoter-like histone modifications renders gene bodies permissive to spurious initiation by RNA polymerase II. This allows previously repressed intragenic regions to acquire promoter-like chromatin features. Cryptic transcription produces aberrant RNAs that interfere with normal gene expression, leading to truncated proteins or nonfunctional mRNAs. The aberrant RNA and protein products impair stem cell self-renewal and differentiation, thereby contributing to the development of aging and disease. This review summarizes the mechanisms underlying age-related cryptic transcription, focusing on the function of H3K36me3, DNA methylation, H3K4me3, H3K27ac, and transcription factors. In addition, we discuss the effects of cryptic transcription on aging stem cells and aged tissues.
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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.