bims-ciryme Biomed News
on Circadian rhythms and metabolism
Issue of 2026–03–08
two papers selected by
Gabriela Da Silva Xavier, University of Birmingham
  1. Endocrine regulation of circadian rhythms.
  2. Restoring circadian rhythms in the hypothalamic paraventricular nucleus reverses aging biomarkers and extends lifespan in male mice.
  1. NPJ Biol Timing Sleep. 2025 Mar 08. pii: 10. [Epub ahead of print]2(1):
    Endocrine regulation of circadian rhythms.
    Kimberly Begemann, Oliver Rawashdeh, Iwona Olejniczak, Violetta Pilorz, Leonardo Vinícius Monteiro de Assis, Jazmin Osorio-Mendoza, Henrik Oster.
      Circadian clocks are internal timekeepers enabling organisms to adapt to recurrent events in their environment - such as the succession of day and night-by controlling essential behaviors such as food intake or the sleep-wake cycle. A ubiquitous cellular clock network regulates numerous physiological processes including the endocrine system. Levels of several hormones such as melatonin, cortisol, sex hormones, thyroid stimulating hormone as well as a number of metabolic factors vary across the day, and some of them, in turn, can feedback on circadian clock rhythms. In this review, we dissect the principal ways by which hormones can regulate circadian rhythms in target tissues - as phasic drivers of physiological rhythms, as zeitgebers resetting tissue clock phase, or as tuners, affecting downstream rhythms in a more tonic fashion without affecting the core clock. These data emphasize the intricate interaction of the endocrine system and circadian rhythms and offer inroads into tissue-specific manipulation of circadian organization.
    DOI:  https://doi.org/10.1038/s44323-025-00024-6
  2. Cell. 2026 Mar 04. pii: S0092-8674(26)00103-0. [Epub ahead of print]
    Restoring circadian rhythms in the hypothalamic paraventricular nucleus reverses aging biomarkers and extends lifespan in male mice.
    Haijiao Zhao, Meimei Liao, Ran Huo, Ting He, Hongni Tian, Zeqi Li, Chen Chen, Ziqing Yu, Juan Chai, Xiaocui Song, Ruichao Shao, Shuhua Ying, Wen Gao, Ling Liu, Di Sang, Qi Li, Haohong Li, Fengchao Wang, Dapeng Ju, Eric Erquan Zhang.
      Age-related circadian disruptions accelerate physiological decline and shorten lifespan. Enhancing circadian amplitude has emerged as a promising strategy for ameliorating age-associated disorders. Here, we show that the circadian-phase-optimized administration of 3'-deoxyadenosine (3dA) strengthens circadian amplitude in hypothalamic paraventricular nucleus (PVN) neurons, mitigates aging biomarkers, and extends mouse lifespan. 3dA restores clock synchrony and hormonal rhythms, including corticosterone, and reduces epigenetic age as measured by DNA methylation clocks. Transcriptomic, hormonal, and epigenetic profiling reveal robust increases in PVN circadian amplitude following timed 3dA administration, and the PVN-specific knockout of RuvB-like ATPase 2 (Ruvbl2) establishes its genetic necessity by abolishing 3dA's benefits. Similarly, chemogenetic PVN activation reproduces 3dA's metabolic and physiological benefits. These findings identify the PVN clock as a pharmacological node linking circadian amplitude to organismal aging, suggest that targeting RUVBL2-dependent circadian transcription enhances network synchrony, and indicate that circadian interventions are promising therapeutic candidates for delaying aging and improving healthspan in aged male mice.
    Keywords:  3′-deoxyadenosine; RUVBL2; aging; amplitude enhancement; circadian rhythms; paraventricular nucleus
    DOI:  https://doi.org/10.1016/j.cell.2026.01.016
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