ReviewThe journal of physiological sciences : JPS2016
Circadian adaptation to cell injury stresses: a crucial interplay of BMAL1 and HSF1.
Review in The journal of physiological sciences : JPS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- CIRCADIAN CLOCK-ASSOCIATED 1 represses thermotolerance by inhibitingHorticulture research · 2026Article
- Morphofunctional State of the Liver Under Conditions of Three-Month Dark Deprivation: The Influence of Circadian Disruptions and Melatonin.International journal of molecular sciences · 2026Article
- Immediate nuclear accumulation of BMAL1 to regulate cellular circadian clock synchronization.Communications biology · 2025Article
- The role of circadian rhythm-related genes in type 2 diabetes from a multi-omics perspective.Journal of global health · 2025Article
- The hidden rhythms of epilepsy: exploring biological clocks and epileptic seizure dynamics.Acta epileptologica · 2025Review
- Role of circadian rhythms in pathogenesis of acute CNS injuries: Insights from experimental studies.Experimental neurology · 2022Review
- Emerging Insight Into the Role of Circadian Clock Gene BMAL1 in Cellular Senescence.Frontiers in endocrinology · 2022Review
- Comprehensive RNA-Seq Profiling Reveals Temporal and Tissue-Specific Changes in Gene Expression in Sprague-Dawley Rats as Response to Heat Stress Challenges.Frontiers in genetics · 2021Article
- Cooperative interaction among BMAL1, HSF1, and p53 protects mammalian cells from UV stress.Communications biology · 2018Article
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
No grant is acknowledged in the PubMed record.
Abstract
The circadian clock system confers daily anticipatory physiological processes with the ability to be reset by environmental cues. This "circadian adaptation system" (CAS), driven by cell-autonomous molecular clocks, orchestrates various rhythmic physiological processes in the entire body. Hence, the dysfunction of these clocks exacerbates various diseases, which may partially be due to the impairment of protective pathways. If this is the case, how does the CAS respond to cell injury stresses that are critical in maintaining health and life by evoking protective pathways? To address this question, here we review and discuss recent evidence revealing life-protective (pro-survival) molecular networks between clock (e.g., BMAL1, CLOCK, and PER2) and adaptation (e.g., HSF1, Nrf2, NF-κB, and p53) pathways, which are evoked by various cell injury stresses (e.g., heat, reactive oxygen species, and UV). The CK2 protein kinase-integrated interplay of the BMAL1 (clock) and HSF1 (heat-shock response) pathways is one of the crucial events in CAS.
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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.