{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T11:45:34Z","timestamp":1785843934467,"version":"3.56.0"},"reference-count":236,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T00:00:00Z","timestamp":1785801600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Chronic obstructive pulmonary disease (COPD) is driven by self-perpetuating inflammation that resists conventional therapies. Recent evidence reveals three interconnected pathogenic layers: immunometabolic reprogramming, m\n                    <jats:sup>6<\/jats:sup>\n                    A epitranscriptomic dysregulation, and excessive NETosis with defective resolution. Pathogenic immune cells shift toward aerobic glycolysis and impaired fatty acid oxidation, sustaining pro-inflammatory phenotypes and corticosteroid resistance. m\n                    <jats:sup>6<\/jats:sup>\n                    A modifications may control the stability of key transcripts such as MALT1, IL-17, and PADI4, as suggested by emerging evidence. A recent rat COPD model study reported that the Shenqi Tiaoshen Formula reduced METTL16-mediated m\n                    <jats:sup>6<\/jats:sup>\n                    A methylation of MALT1, though human replication is lacking. Concurrently, neutrophil extracellular traps (NETs) damage lung tissue and expose autoantigens, accompanied by failed resolution. Traditional Chinese Medicine (TCM)\u2014including Shenqi Tiaoshen Formula, baicalin, berberine, astragaloside IV, and curcumin\u2014can reprogram metabolism via AMPK, modulate m\n                    <jats:sup>6<\/jats:sup>\n                    A writers\/erasers, inhibit NETosis, and upregulate SPMs in preclinical models. However, most evidence derives from non-COPD models or uses supraphysiological concentrations; the translational gap to human COPD remains substantial. We discuss the bidirectional metabolism-m\n                    <jats:sup>6<\/jats:sup>\n                    A crosstalk as a theoretical framework requiring experimental validation, and outline single-cell m\n                    <jats:sup>6<\/jats:sup>\n                    A sequencing, spatial metabolomics, and CRISPR screening as tools to accelerate precision TCM for COPD.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1904338","type":"journal-article","created":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T11:08:53Z","timestamp":1785841733000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Epitranscriptomics, immunometabolism, and NETosis: unlocking novel mechanisms of traditional Chinese medicine in COPD"],"prefix":"10.3389","volume":"17","author":[{"given":"Hui-Hui","family":"Chen","sequence":"first","affiliation":[{"name":"Zhuhai Hospital of Integrated Traditional Chinese and Western 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