{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T22:34:06Z","timestamp":1790202846402,"version":"4.1.0"},"reference-count":68,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T00:00:00Z","timestamp":1765238400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T00:00:00Z","timestamp":1765238400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["aocs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Lipids"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>This in silico network\u2010pharmacology investigation delineates the molecular interplay linking statin\u2010induced Coenzyme Q10 (CoQ10) deficiency to statin\u2010associated muscle symptoms (SAMS). GeneCards\u2010derived targets related to SAMS, CoQ10 deficiency, and statins were integrated, and the intersecting gene set was analyzed through STRING\u2010based protein\u2013protein interaction mapping, followed by hub\u2010gene prioritization using CytoHubba. Functional enrichment via ShinyGO revealed that the 145 common genes converge predominantly on inflammatory, metabolic, and mitochondrial pathways. Tumor necrosis factor (TNF) emerged as a principal regulatory node, exerting influence through Mitogen\u2010Activated Protein Kinase (MAPK)\u2010mediated apoptotic and stress\u2010response cascades that plausibly contribute to mitochondrial dysfunction, oxidative stress, impaired energy metabolism, and myocellular injury in the context of CoQ10 depletion. The constructed pathway\u2010based interaction network illustrates how suppression of the mevalonate pathway by statins disrupts CoQ10 biosynthesis, sensitizing muscle tissue to cytokine\u2010driven inflammatory signaling and amplifying apoptotic susceptibility. Collectively, the findings highlight the TNF\u2013MAPK axis as a mechanistic core of SAMS pathophysiology and underscore the interconnected roles of immune activation, lipid metabolic imbalance, and mitochondrial impairment. These insights provide a molecular rationale for therapeutic strategies targeting mitochondrial preservation or inflammatory modulation, including CoQ10 supplementation, and reinforce the need for experimental and clinical validation to substantiate computationally derived predictions.<\/jats:p>","DOI":"10.1002\/lipd.70028","type":"journal-article","created":{"date-parts":[[2025,12,10]],"date-time":"2025-12-10T04:35:52Z","timestamp":1765341352000},"page":"299-307","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Network Pharmacology Insights Into Statin\u2010Induced Coenzyme\n                    <scp>Q10<\/scp>\n                    Deficiency: Lipid Metabolic Crosstalk,\n                    <scp>TNF<\/scp>\n                    \u2013\n                    <scp>MAPK<\/scp>\n                    Signaling, and Muscle 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