Circadian adaptation to cell injury stresses: a crucial interplay of BMAL1 and HSF1.
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.
['Tamaru|Teruya|T|', 'Ikeda|Masaaki|M|']
D056930:ARNTL Transcription Factors D000222:Adaptation, Physiological D000818:Animals D057906:Circadian Clocks D002940:Circadian Rhythm D006360:Heat-Shock Proteins D006801:Humans D018384:Oxidative Stress D017382:Reactive Oxygen Species
Adaptation Circadian clock Heat shock Oxidative stress Protein kinase