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--- inflammatory_proteins [2025/07/09 14:54] – [The Causal Effects Between Circulating Inflammatory Proteins and Osteoarthritis: A Mendelian Randomization and Transcriptomic Analysis] administrador
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     * [[cancer]] progression
-===== The Causal Effects Between Circulating Inflammatory Proteins and Osteoarthritis: A Mendelian Randomization and Transcriptomic Analysis =====
-In a bidirectional two-sample [[Mendelian randomization]] and [[transcriptomic analysis]]
-Lin et al.
-from the Xiangya Hospital, Changsha
-published in the Journal of Pain Research
-to investigate the causal relationship between circulating inflammatory proteins and [[osteoarthritis]] (OA) using Mendelian randomization and transcriptomic data.
-The study suggests causal roles for various inflammatory proteins in [[osteoarthritis pathogenesis]]. Certain proteins (e.g., interleukin-8, fractalkine) are associated with higher OA risk, while others (e.g., interleukin-10 receptor subunit alpha) correlate with lower risk. Additionally, OA itself may causally influence inflammatory protein levels, particularly in a joint-specific manner (hip vs knee). Six key OA-related inflammation-related genes (IRGs) were identified as potential biomarkers
-((Lin S, Wu C, Pan Y. The Causal Effects Between Circulating [[Inflammatory Proteins]] and [[Osteoarthritis]]: A [[Mendelian Randomization]] and [[Transcriptomic Analysis]]. J Pain Res. 2025 Jul 4;18:3383-3402. doi: 10.2147/JPR.S523677. PMID: 40630929; PMCID: PMC12236367.)).
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-**Critical Review:**
-This study leverages the strengths of two-sample [[Mendelian Randomization]] (MR) to address directionality in inflammation-OA associations, bolstered by transcriptomic analysis. However, several issues warrant scrutiny:
-- **Causality overreach:** While MR reduces confounding, it still relies on assumptions (e.g., no pleiotropy), which are not exhaustively addressed here. The evidence remains "suggestive" rather than definitive.
-- **Protein-level resolution:** Using summary GWAS data for circulating proteins imposes a limit on biological granularity. There's no validation through proteomic assays or replication in independent cohorts.
-- **Transcriptomic correlation does not imply function:** Identifying differentially expressed genes does not establish them as pathologically relevant without mechanistic data.
-- **Statistical multiple-testing:** Given the number of proteins and genes tested, the absence of a clear correction method or false discovery rate control weakens confidence in individual associations.
-- **Clinical relevance:** The clinical applicability remains speculative; no risk stratification models or therapeutic implications are drawn from the biomarkers.
-**Final Verdict:** A conceptually valuable study with well-executed bioinformatics and MR methodology, yet weakened by overinterpretation, limited functional validation, and uncertain translational impact.
-**Takeaway for Neurosurgeons:** While the findings are not directly actionable, the study underscores the growing relevance of systemic inflammation in joint pathology—potentially informing holistic care in spine patients with concurrent OA.
-**Bottom Line:** A hypothesis-generating MR study suggesting bidirectional causal links between inflammatory proteins and OA, but lacking translational depth.
-**Rating:** 5.5 / 10
-**Categories:** Osteoarthritis, Basic Science, Inflammation, Genomics
-**Tags:** osteoarthritis, Mendelian randomization, inflammatory biomarkers, transcriptomics, cytokines, genomics, neuroinflammation