ArticleScience advances2025
The inflammatory and genetic mechanisms underlying the cumulative effect of co-occurring pain conditions on depression.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07480460 (Frontostriatal Connectivity and Gene Expression in Exercise-induced Relief of Back Pain), which is not on this map. Cited by 16 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
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.
Frontostriatal Connectivity and Gene Expression in Exercise-induced Relief of Back Pain
Who cites it
16 citing papers in PubMed.
- IL-1α and CRP as key inflammatory mediators linking neuropathic pain, anxiety, and depression in major depressive disorder.BMC psychiatry · 2026Article
- Prevalence of Chronic Pain and Associated Factors Among Nursing Students in Heilongjiang Province, China: A Cross-Sectional Study.Nursing open · 2026Article
- The metabolomic signatures mediate associations between physical frailty and metabolic dysfunction-associated steatotic liver disease.Science advances · 2026Article
- Multimodal fusion of brain imaging and proteomics reveals a brain-body pathway linking depression and metabolic dysfunction.Psychological medicine · 2026Article
- Sarcopenia as a risk factor for incident pain in Chinese middle-aged and older adults: longitudinal evidence from the CHARLS cohort.The journal of nutrition, health & aging · 2026Article
- Timing of depressive episode onset relative to chronic pain reveals distinct patterns of affective and multisite pain.Frontiers in psychiatry · 2026Article
- The Impact of Catastrophization and Emotions on Pain: A Narrative Review of Underlying Mechanisms.Journal of pain research · 2026Review
- Multisite Chronic Pain Reveals Neuro-Immune-Metabolic Dysregulation across Rheumatoid Arthritis and Depression.Research (Washington, D.C.) · 2026Article
- Acoustic stimulation in pain management: neurobiological mechanisms and clinical applications-a narrative review.Frontiers in neuroscience · 2026Review
- Association of inflammatory bowel disease with cardiovascular disease, and the mediating role of inflammation: a matched-cohort study.Therapeutic advances in gastroenterology · 2026Article
- Chronic Pain and Newly Reported Frequent Feelings of Depression: A Nationally Representative Longitudinal Study in 2019-2020.Journal of pain research · 2026Article
- Patterns of multimorbidity among low-income adults who smoke with implications for tailored interventions: a cluster analysis using a Mixture of Bernoulli model.Frontiers in medicine · 2026Article
- CRH neurons in the AM-ACC circuit drive chronic pain and anxiety comorbidity.Frontiers in neuroscience · 2026Article
- Metabolic Syndrome and Low Back Pain: Evidence from Cross-Sectional and Mendelian Randomization Analysis.Journal of pain research · 2026Article
- Influencing factors of depressive symptoms in middle-aged and elderly people and its regional differences in china: a study based on Bayesian network model.Journal of health, population, and nutrition · 2025Article
- Depression as an Independent Predictor of Incident Pain: Longitudinal Evidence From CHARLS.Journal of pain research · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic pain conditions frequently coexist and share common genetic vulnerabilities. Despite evidence showing associations between pain and depression, the additive effect of co-occurring pain conditions on depression risk and the underlying mechanisms remain unclear. Leveraging data from 431,038 UK Biobank participants with 14-year follow-up, we found a significantly increased risk of depression incidence in individuals reporting pain, irrespective of body site or duration (acute or chronic), compared with pain-free individuals. The depression risk increased with the number of co-occurring pain sites. Mendelian randomization supported potential causal inference. We constructed a composite pain score by combining individual effects of acute or chronic pain conditions across eight body sites in a weighted manner. We found that depression risks increased monotonically in parallel with composite pain scores. Moreover, some inflammatory markers, including C-reactive protein, partially mediated the association between composite pain scores and depression risk. Considering the high prevalence of comorbid depression and pain, pain screening may help identify high-risk individuals for depression.
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