ArticleCurrent research in microbial sciences2026
Circadian rhythms regulate osteoclast recycling through gut microbiota-dependent Th17 cell expansion.
Article in Current research in microbial sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
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Who cites it
4 citing papers in PubMed.
- Why Do We Lose Bone During Weight Loss: Can It Be Prevented?Current osteoporosis reports · 2026Review
- Rhythmic Metabolism in Osteosarcopenia: Emerging Evidence, a Chronometabolomic Framework for the Bone-Muscle Unit, and Research Priorities.Metabolites · 2026Review
- Circadian control of immune homeostasis in cardiovascular health and disease.Frontiers in immunology · 2026Review
- Nutritional adaptation to circadian misalignment: implications for musculoskeletal health in modern lifestyles.Frontiers in nutrition · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The circadian clock coordinates diverse biological processes to maintain physiological function and homeostasis in mammals under the day-night light cycle. Disruption of circadian rhythms impairs immune and metabolic functions and increases susceptibility to various diseases. Here, we demonstrate that long-term rest-phase time-restricted feeding (TRF), which disrupts circadian rhythmicity, induces bone loss and gut microbiota dysbiosis in male mice. Fecal microbiota transplantation (FMT) from circadian-misaligned feeding donors to germ-free recipients increased Th17 cell populations, thereby promoting the fusion of osteomorphs-a recently identified osteoclast precursor-into mature osteoclasts through the RANKL-RANK-OPG signaling pathway. Collectively, our findings identify a gut microbiota-Th17-osteomorph axis as a critical mediator of circadian disruption-induced bone loss, uncovering a previously unrecognized mechanism by which circadian rhythms regulate skeletal homeostasis.
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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.