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One possible pathological mechanism underlying hypertension and its related health consequences is dysfunction of the circadian system-a network of coupled circadian clocks that generates and orchestrates rhythms of ≈24 h in behavior and physiology. To better understand the role of circadian function during the development of hypertension, circadian regulation of motor activity is investigated in spontaneously hypertensive rats (SHRs) before the onset of hypertension and in their age-matched controls-Wistar Kyoto rats (WKYs). Two complementary properties in locomotor activity fluctuations are examined to assessthe multiscale regulatory function of the circadian control network: 1) rhythmicity at ≈24 h and 2) fractal patterns-similar temporal correlation at different time scales (≈0.5-8 h). Compared to WKYs, SHRs have more stable and less fragmented circadian activity rhythms but the changes in the rhythms (e.g., period and amplitude) from constant dark to light conditions are reduced or opposite. SHRs also have altered fractal activity patterns, displaying activity fluctuations with excessive regularity at small timescales that are linked to rigid physiological states. These different rhythmicity/fractal patterns and their different responses to light in SHRs indicate that an altered circadian function may be involved in the development of hypertension.
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http://dx.doi.org/10.1002/adbi.202200324 | DOI Listing |
Stroke
September 2025
Departments of Radiology and Neurology, Neuroprotection Research Laboratories, Massachusetts General Hospital, Harvard Medical School, Boston (E.L., R.M.P., K.H., E.H.L., E.E.).
Background: Despite promising preclinical results, remote limb ischemic postconditioning efficacy in human stroke treatment remains unclear, with mixed clinical trial outcomes. A potential reason for translational difficulties could be differences in circadian rhythms between nocturnal rodent models and diurnal humans.
Methods: Male C57BL/6J mice were subjected to transient focal cerebral ischemia and then exposed to remote postconditioning during their active or inactive phase and euthanized at 24 hours and 3 days.
Nat Commun
September 2025
Centre for Genomics and Oncological Research (GENYO), Avenue de la Ilustración 114, 18016, Granada, Spain.
Circadian oscillations of gene transcripts rely on a negative feedback loop executed by the activating BMAL1-CLOCK heterodimer and its negative regulators PER and CRY. Although circadian rhythms and CLOCK protein are mostly absent during embryogenesis, the lack of BMAL1 during prenatal development causes an early aging phenotype during adulthood, suggesting that BMAL1 performs an unknown non-circadian function during organism development that is fundamental for healthy adult life. Here, we show that BMAL1 interacts with TRIM28 and facilitates H3K9me3-mediated repression of transposable elements in naïve pluripotent cells, and that the loss of BMAL1 function induces a widespread transcriptional activation of MERVL elements, 3D genome reorganization and the acquisition of totipotency-associated molecular and cellular features.
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September 2025
Department of Psychosocial Research and Epidemiology, The Netherlands Cancer Institute - Antoni van Leeuwenhoek Hospital, Amsterdam, The Netherlands
Objectives: Night shift work has been classified as probably carcinogenic to humans, possibly related to suppression of melatonin secretion. Although experimental studies suggest that melatonin inhibits intestinal tumor proliferation, epidemiological evidence for a relationship between night shift work and colorectal cancer (CRC) risk is lacking.
Methods: We prospectively examined the association between night shift work and CRC in the Nightingale Study.
BMJ Health Care Inform
September 2025
Center for Sleep and Circadian Medicine, The Affiliated Brain Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China
Objectives: The objectives were to examine the associations between accelerometer-measured circadian rest-activity rhythm (CRAR), the most prominent circadian rhythm in humans and the risk of mortality from all-cause, cancer and cardiovascular disease (CVD) in patients with cancer.
Methods: 7456 cancer participants from the UK Biobank were included. All participants wore accelerometers from 2013 to 2015 and were followed up until 24 January 2024, with a median follow-up of 9.
Metab Syndr Relat Disord
September 2025
Yale School of Medicine, New Haven, Connecticut, USA.
Poor sleep has been identified as a strong risk factor for metabolic syndrome. Shift workers, who often experience reduced and misaligned sleep due to nighttime work schedules, are particularly susceptible to both sleep disturbances and metabolic syndrome. However, the interplay among shift work, sleep disturbances, and metabolic syndrome remains insufficiently explored.
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