# Advances in Traditional Chinese Medicine for chronic obstructive pulmonary disease through multi-omics approaches

**Authors:** Kun Yang, Jun Wang, Yizhao Ma, Hailong Zhang

PMC · DOI: 10.3389/fcell.2026.1761374 · Frontiers in Cell and Developmental Biology · 2026-01-28

## TL;DR

This paper reviews how multi-omics technologies are helping to understand and improve Traditional Chinese Medicine treatments for COPD.

## Contribution

The paper systematically summarizes recent advances in using multi-omics to elucidate the mechanisms and effectiveness of TCM for COPD.

## Key findings

- Multi-omics approaches reveal molecular mechanisms and biomarkers for TCM treatment of COPD.
- Network pharmacology and pharmacogenomics help predict component-target interactions in TCM formulas.
- Metabolomics and microbiomics uncover lung-gut axis regulation and metabolic changes in COPD.

## Abstract

Chronic obstructive pulmonary disease (COPD) is a common and complex heterogeneous chronic inflammatory airway disorder characterized by multifactorial pathogenesis and limited therapeutic options. It remains one of the leading causes of morbidity and mortality worldwide, severely impairing patients’ quality of life and life expectancy. Traditional Chinese Medicine (TCM), with its holistic perspective, syndrome differentiation, and multi-component formulations, is widely used in the adjunctive treatment and rehabilitation of COPD. Evidence suggests that TCM can relieve symptoms, reduce acute exacerbations, and enhance quality of life. However, the “multi-component-multi-target-multi-pathway” nature of TCM formulas has long made their mechanisms difficult to systematically elucidate. In recent years, the rapid development of high-throughput multi-omics technologies has provided unprecedented opportunities to decipher the systems biology mechanisms underlying TCM treatment of COPD. Multi-dimensional data from network pharmacology, genomics, transcriptomics, proteomics, metabolomics, and microbiomics can comprehensively reveal disease-related molecular changes. These findings provide scientific evidence for the objectification of TCM syndromes, the identification of biomarkers, and the clarification of multi-target mechanisms in key herbal formulas, such as Bufei Jianpi granules. Moreover, multi-omics studies have also promoted exploration of emerging fields such as the “lung-gut axis”, providing new theoretical perspectives for understanding the complex pathological processes of COPD. This review systematically summarizes recent advances in TCM-based prevention and treatment of COPD using multi-omics strategies. Key progress includes the application of network pharmacology and pharmacogenomics in component-target prediction, the role of transcriptomics/proteomics in molecular target validation, and the value of metabolomics and microbiomics in uncovering metabolic reprogramming and lung-gut axis regulation. Integrated multi-omics approaches also demonstrate significant potential in biomarker discovery and the development of precision TCM. In addition, this review provides a critical evaluation of current trends, potential breakthroughs, challenges, and opportunities in advancing TCM from empirical medicine toward evidence-based and precision medicine, aiming to offer systematic and comprehensive theoretical foundations and research perspectives for TCM-based COPD therapy.

## Linked entities

- **Diseases:** chronic obstructive pulmonary disease (MONDO:0005002), COPD (MONDO:0005002)

## Full-text entities

- **Genes:** Mmp9 (matrix metallopeptidase 9) [NCBI Gene 81687], SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}, Timp1 (TIMP metallopeptidase inhibitor 1) [NCBI Gene 116510] {aka TIMP-1, Timp}, Zhx2 (zinc fingers and homeoboxes 2) [NCBI Gene 387609] {aka Afr-1, Afr1, Raf, mKIAA0854}, SMAD2 (SMAD family member 2) [NCBI Gene 4087] {aka CHTD8, JV18, JV18-1, LDS6, MADH2, MADR2}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, Rela (Rela proto-oncogene, NFKB subunit) [NCBI Gene 19697] {aka p65, p65 NF-kappa B, p65 NFkB}, MAPK3 (mitogen-activated protein kinase 3) [NCBI Gene 5595] {aka ERK-1, ERK1, ERT2, HS44KDAP, HUMKER1A, P44ERK1}, SERPINE1 (serpin family E member 1) [NCBI Gene 5054] {aka PAI, PAI-1, PAI1, PLANH1}, Jak1 (Janus kinase 1) [NCBI Gene 84598], HIF1A (hypoxia inducible factor 1 subunit alpha) [NCBI Gene 3091] {aka HIF-1-alpha, HIF-1A, HIF-1alpha, HIF1, HIF1-ALPHA, MOP1}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468] {aka CIMT1, FPLD3, GLM1, NR1C3, PPARG1, PPARG2}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, STAT5A (signal transducer and activator of transcription 5A) [NCBI Gene 6776] {aka MGF, STAT5}, Stat3 (signal transducer and activator of transcription 3) [NCBI Gene 25125], TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}, Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}, Mapk14 (mitogen-activated protein kinase 14) [NCBI Gene 26416] {aka CSBP2, Crk1, Csbp1, Mxi2, PRKM14, PRKM15}, Sirt1 (sirtuin 1) [NCBI Gene 309757] {aka Sir2}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, Mapk8 (mitogen-activated protein kinase 8) [NCBI Gene 26419] {aka JNK, JNK1, Prkm8, SAPK1}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, Sirt1 (sirtuin 1) [NCBI Gene 93759] {aka SIR2L1, Sir2, Sir2a, Sir2alpha}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, Egfr (epidermal growth factor receptor) [NCBI Gene 13649] {aka 9030024J15Rik, Erbb, Errb1, Errp, Wa5, wa-2}, Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}
- **Diseases:** osteoporosis (MESH:D010024), toxicity (MESH:D064420), gastrointestinal disorders (MESH:D005767), cardiovascular diseases (MESH:D002318), acute tissue injury (MESH:D001930), emphysematous destruction (MESH:D041882), limitation (MESH:D045745), intestinal excess syndrome (MESH:D007410), immune dysregulation (OMIM:614878), pulmonary fibrosis (MESH:D011658), dysfunction (MESH:D006331), exacerbation (MESH:D018450), TCM (MESH:C562377), inflammatory cytokines (MESH:D000080424), bacterial infection (MESH:D001424), musculoskeletal dysfunction (MESH:D009140), emphysema (MESH:D004646), lung deficiency syndrome (MESH:D055370), lung (MESH:D008171), lung cancer (MESH:D008175), PD (MESH:D010300), mitochondrial dysfunction (MESH:D028361), fibrosis (MESH:D005355), respiratory infections (MESH:D012141), Inflammation (MESH:D007249), inflammatory dysregulation (MESH:D021081), airway and/or alveolar abnormalities (MESH:D000402), impaired energy metabolism (MESH:D008659), chronic airway and pulmonary inflammation (MESH:D011014), AECOPD (MESH:D029424), inflammatory lung disorder (MESH:D016726), lung-kidney deficiency syndromes (MESH:C537292)
- **Chemicals:** MDA (MESH:D008315), phenylalanine (MESH:D010649), peimine (MESH:C014242), amino acid (MESH:D000596), carnitine (MESH:D002331), unsaturated fatty acid (MESH:D005231), hypotaurine (MESH:C003949), bile acids (MESH:D001647), acacetin (MESH:C023717), -Ping-Feng-San (-), short-chain fatty acid (MESH:D005232), flavonoids (MESH:D005419), tryptophan (MESH:D014364), lysophosphatidylcholines (MESH:D008244), sphingolipid (MESH:D013107), AST (MESH:C052064), naringenin (MESH:C005273), lipopolysaccharide (MESH:D008070), lipid (MESH:D008055), citric acid (MESH:D019343), steroid (MESH:D013256), taurine (MESH:D013654), pterostilbene (MESH:C107773), choline (MESH:D002794), quercetin (MESH:D011794), nobiletin (MESH:C008661), GTP (MESH:D006160), GDP (MESH:D006153), isoliquiritigenin (MESH:C040920), terpenoids (MESH:D013729), arachidonic acid (MESH:D016718), hesperetin (MESH:C013015), tyrosine (MESH:D014443), phospholipid (MESH:D010743)
- **Species:** Bifidobacterium (genus) [taxon 1678], Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116], Mus musculus (house mouse, species) [taxon 10090], Rheum palmatum (species) [taxon 137221], Rheum tanguticum (species) [taxon 137226]

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## References

65 references — full list in the complete paper: https://tomesphere.com/paper/PMC12929911/full.md

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Source: https://tomesphere.com/paper/PMC12929911