Table 1 The role of necroptosis in small-airway disease and emphysema.

From: Role of necroptosis in airflow limitation in chronic obstructive pulmonary disease: focus on small-airway disease and emphysema

Study	Research objects	Group	Necroptosis indicators	Small-airway disease indicators	Emphysema indicators
Wang Y, 2018	HBE cells	EG: Nec-1 + CSE CG: DMSO + CSE	/	IL6, IL8, MUC5AC ↓	/
XU F, 2018	HBE cells	EG: Nec-1/GSK'872 + PM CG: DMSO + PM	PI-positive cells↓	IL6, IL8, MUC5AC ↓	/
XU F, 2018	Male C57BL/6 mice (aged 6-8 weeks)	EG: Nec-1 + PM CG: DMSO + PM	/	Total inflammatory cells, neutrophils↓ MUC5AC, CXCL1, CXCL2, G-CSF ↓ Inflammation score↓	/
LUAN G, 2022	BEAS-2B cells	EG: TF-3 + CSE CG: CSE	/	TNF-α, IL-6, IL-1β ↓	/
	BEAS-2B cells	EG: TF-3 + CSE + z-VAD Nec-1 + CSE + z-VAD CG: CSE + z-VAD	p-RIPK3, p-MLKL ↓ PI-positive cells↓ Necroptotic rate↓	/	/
	Male C57BL/6 J mice (aged 7 weeks)	EG: TF-3 + CSE CG: CSE	p-RIPK3, p-MLKL ↓	TNF-α, IL-1β ↓	Emphysematous changes, MLI, DI ↓
Wang Y, 2020	BMDM cells	EG: Nec-1 + CSE GSK'872 + CSE CG: DMSO + CSE	/	CXCL1, CXCL2, IL-6↓	/
CHEN D, 2021	MLE-12 cells cocultured with BMDMs	EG: GSK'872 + CSE Z-VAD + CSE CG: CSE	/	HMGB1, TNF-α, IL-6 (GSK'872) ↓ (Z-VAD) ↑	/
CHEN D, 2021	Female C57BL/6 J mice (aged 6 weeks)	EG: GSK'872 + Smoke Z-VAD + Smoke CG: DMSO + Smoke	p-MLKL(GSK'872) ↓	HMGB1, IL-6 (GSK'872) ↓ Neutrophils, CD8⁺ T cells, macrophage (GSK'872) ↓	Lung chord lengths, alveolar area (GSK'872) ↓
POUWELS S D, 2016	Female BALB/cByJ mice (aged 8 weeks)	EG: Nec-1 + Smoke CG: DMSO + Smoke	/	Neutrophils, MPO ↓	/
MAO K, 2021	Male C57BL/6 mice (aged 8 weeks)	EG: Melatonin + LPS CG: LPS	p-RIPK3, p-MLKL ↓ RIP1, RIP3, MLKL ↓	Airway wall thickness, BALT ↓ cilium number of bronchial epithelial cells↑ IL-1α, IL-1β, TNF-α, ICAM-1, CXCL10, G-CSF ↓ CD4⁺, CD8⁺, CD45⁺ T cells, NK cells, CD11b⁺, CD11c⁺, F4/80⁺ macrophages↓	Alveolar enlargement↓ lung destruction area↓
LU Z, 2021	Acute CS-exposure mice	EG: RIPK3−/− mice CG: WT mice	RIPK3 deletion	Mip1a↓ Total leukocytes, neutrophils, lymphocytes ↓	/
	Acute CS-exposure mice	EG: MLKL^−/− mice CG: WT mice	MLKL deletion	Total leukocytes, neutrophils↓ CXCL1, Mmp12, Ym1, Marco↓	/
	Chronic CS-exposure mice	EG: RIPK3^−/− mice MLKL^−/− mice CG: WT mice	RIPK3 deletion (RIPK3^−/−) MLKL deletion (MLKL^−/−)	Total leukocytes, Alveolar macrophage↓ Collagen deposition↓ Ym1↓ Airway inflammation score, Epithelial thickness↓ Marco (RIPK3^−/−) ↓ lymphocytes (RIPK3^−/−) ↓ CXCL1, Mmp12, Mmp8 (MLKL^−/−) ↓ macrophages, neutrophils (MLKL^−/−) ↓	MLI ↓ Mmp12 (MLKL^−/−) ↓

↑, The data of the experimental group was significantly higher than that of the control group; ↓, The data of the experimental group was significantly lower than that of the control group; /, There is no relevant expression in this paper; −/−, Gene deletion.
BALT bronchus-associated lymphoid tissue, BEAS-2B human normal lung epithelial cells, BMDM bone marrow–derived macrophages, CG control group, CSE cigarette smoke extract, CXCL CXC chemokine ligand, DI destructive index, DMSO dimethyl sulfoxide, EG experimental group, G-CSF granulocyte-colony stimulating factor, HBE human bronchial epithelial cells, HMGB1 high-mobility group box-1, ICAM-1 circulating intercellular adhesion molecule-1, IL interleukin, LPS lipopolysaccharide, MLE-12 mouse lung epithelial cells, MLI mean linear intercept, MLKL mixed-lineage kinase domain-like, MPO myeloperoxidase, PM particulate matter, RIPK receptor-interacting protein kinase, TF-3 theaflavin-3,3′-digallate, TNF tumour necrosis factor, WT wild type.

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Table 1 The role of necroptosis in small-airway disease and emphysema.

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