SynthesisNeuroscience and biobehavioral reviews2021
Glucocorticoid resistance and β2-adrenergic receptor signaling pathways promote peripheral pro-inflammatory conditions associated with chronic psychological stress: A systematic review across species.
Synthesis in Neuroscience and biobehavioral reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Chronic stress in relation to clinical burnout: an integrative scoping review of definitions and measurement approaches.Frontiers in psychology · 2025Pooled it
- Comorbidities and Inflammation: How Chronic Diseases Prime the Host Response in Sepsis.International journal of molecular sciences · 2026Review
- Terpenes as Potential Multi-Target Modulators of Chronic Stress-Induced Neuroendocrine-Immune Dysregulation.International journal of molecular sciences · 2026Review
- Biomolecular Pathways Linking Preoperative Chronic Stress to Postoperative Cardiovascular Dysfunction in Noncardiac Surgery.Biomolecules · 2026Review
- Review
- Glucocorticoid signalling dysregulation and immune cell adaptation in Anorexia Nervosa.Molecular psychiatry · 2026Article
- Stress and the Immune System: Insights From Psychoneuroimmunology.Physiological research · 2026Review
- Combined effects of social health and long-term exposure to fine particulate matter on cardiovascular disease in Chinese middle-aged and older adults.Social psychiatry and psychiatric epidemiology · 2026Article
- Dose as a fundamental organizing principle in physiology: Implications for mechanism, disease, and precision medicine.Journal of precision medicine (Amsterdam, Netherlands) · 2026Article
- Review
- A Neuroendocrine-Immune Model of Hidradenitis Suppurativa: Mechanistic Insights into Pain, Pruritus, and Hormonal Triggers.Journal of clinical medicine · 2026Review
- A Stress-Neuroendocrine-Myeloid Inflammation Axis Is Associated with the Progression of Ménière's Disease.Brain, behavior, & immunity - health · 2026Article
- Perinatal hyperandrogenization and immune activation in rodents model subtypes of autism.Translational psychiatry · 2026Article
- Male Stress Is Associated with Ovarian and Endometrial Responses in ICSI Cycles: Is Seminal Plasma the Linchpin?International journal of molecular sciences · 2026Article
- Human placental extract, melsmon, suppresses stress-induced neuroinflammation and peripheral inflammation in a mouse model of depression.Frontiers in pharmacology · 2026Article
- Corticotropin-releasing factor (CRF) in brain aging: from mitochondrial dysfunction to inflammaging.Frontiers in aging neuroscience · 2026Review
- Psychological stress and gut microbiota regulation of osteoarthritis progression: mechanisms and therapeutic strategies.Frontiers in microbiology · 2026Review
- The Impact of Catastrophization and Emotions on Pain: A Narrative Review of Underlying Mechanisms.Journal of pain research · 2026Review
- Stress-induced IL-6 regulation in pediatric bone growth disorders: current insights and therapeutic strategies.Frontiers in endocrinology · 2026Review
- The interplay between stress, inflammation and Parkinson's disease: insights from the COVID-19 pandemic.NPJ Parkinson's disease · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Activation of the HPA-axis and SNS are widely accepted to link chronic stress with elevated levels of peripheral pro-inflammatory markers in blood. Yet, empirical evidence showing that peripheral levels of glucocorticoids and/or catecholamines mediate this effect is equivocal. Recent attention has turned to the possibility that cellular sensitivity to these ligands may contribute to inflammatory mediators that accompany chronic stress. We review current evidence for the association of chronic stress with glucocorticoid receptor (GR) and β-adrenergic receptor (β-AR) signaling sensitivity. Across 15 mouse, 7 primate, and 19 human studies, we found that chronic stress reliably associates with downregulation in cellular GR sensitivity, alterations in intracellular β-AR signaling, and upregulation in pro-inflammatory biomarkers in peripheral blood. We also present evidence that alterations in GR and β-AR signaling may be specific to myeloid progenitor cells such that stress-related signaling promotes release of cells that are inherently less sensitive to glucocorticoids and differentially sensitive to catecholamines. Our findings have broad implications for understanding mechanisms by which chronic stress may contribute to pro-inflammatory phenotypes.
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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.