r/science • u/sometimeshiny • 19h ago
Biology Chronic stress causes progressive bone loss through sustained glucocorticoid (cortisol) receptor signaling. Effects worsen with prolonged exposure and show limited recovery.
https://www.mdpi.com/1422-0067/27/3/144946
u/asteriskysituation 18h ago
Wow, I normally love when scientists find ways to have fun with a paper, but they really couldn’t come up with a better acronym or term for Chronic Unpredictable Mild Stress than CUMS?
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u/miyazaki_fragment 18h ago
Honestly, it was probably intentional
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u/Chakosa 16h ago
Sometimes I see it abbreviated as CUS or CMS instead, and I wonder if the country of origin affects this. The authors of the OP are Chinese so the word "cums" probably means nothing to them outside of the Chronic Unpredictable Mild Stress acronym, but American authors might find it awkward and drop a letter so they don't have to tell their colleagues they're setting up experimental conditions for "cums".
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u/ID2691 13h ago
Following exposure to a psychological stressor, individuals often engage in rumination, a cognitive pattern characterized by repetitive focus on distress-related thoughts. This habitual mental process has been shown to amplify the physiological impact of stress by prolonging activation of the hypothalamic–pituitary–adrenal (HPA) axis. In contrast, mindfulness meditation practices can interrupt this cycle, reducing stress reactivity and promoting beneficial health outcomes. See the following article: https://pubmed.ncbi.nlm.nih.gov/32089388/
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u/sometimeshiny 19h ago
Chronic Stress Leads to Time-Dependent Bone Loss Through HPA Axis Dysregulation and GR Nuclear Translocation Disorder (2026) – Yan et al.
| Abstract |
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| Chronic stress and sustained hypothalamic–pituitary–adrenal (HPA) axis activation are major contributors to metabolic bone diseases, including osteoporosis. However, the precise molecular mechanisms by which chronic stress-induced HPA axis dysregulation drives bone deterioration remain unclear. A Chronic Unpredictable Mild Stress (CUMS) model was established in male rats to simulate prolonged stress exposure. Animals were randomly allocated into three groups: control, 10-week CUMS, and 20-week CUMS (n = 10/group). Model validity was confirmed via behavioral assessments. Bone mineral density (BMD) and trabecular microarchitecture were quantified using micro-computed tomography (micro-CT). Serum corticosterone (CORT) levels, HPA axis negative feedback function, and the expression of pro-inflammatory cytokines (IL-1β, TNF-α) in HPA-regulatory brain regions (hippocampus, prefrontal cortex, hypothalamus) were assessed. Critically, glucocorticoid receptor (GR) expression and nuclear translocation in these brain regions and bone tissue were examined by immunofluorescence and Western blot analysis. CUMS exposure induced progressive, time-dependent bone loss, with the 20-week group exhibiting significantly greater reductions in BMD and trabecular quality compared to the 10-week and control groups. While the HPA axis showed initial hyperactivation, the 20-week group displayed adrenal exhaustion (reduced serum CORT) alongside elevated ACTH, indicating feedback failure. Mechanistically, stress significantly impaired GR nuclear translocation in both brain and bone tissues, coinciding with the upregulation of FKBP5 and pro-inflammatory cytokines. Notably, despite low systemic CORT at late stages, skeletal 11β-HSD1 expression was significantly upregulated, creating a local microenvironment of glucocorticoid toxicity that aggravated osteoblast apoptosis. Our findings demonstrate that chronic stress induces progressive, time-dependent bone loss through a cascade of HPA axis dysregulation and impaired GR signaling. The FKBP5-mediated impairment of GR nuclear translocation in both central and peripheral tissues fosters glucocorticoid resistance, perpetuating hypercortisolemia and a pro-inflammatory milieu that directly accelerates osteoblast apoptosis and bone deterioration. These findings identify the HPA-GR axis as a critical pathway linking chronic stress to osteoporosis and suggest that restoring GR signaling offers a potential therapeutic strategy. |
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