Inflammation is a defense mechanism that the immune system uses in response to harmful stimuli such as pathogens, damaged cells, toxic compounds, or irradiation. These stimuli may induce inflammatory response and potentially tissue damage in respiratory, cardiovascular, digestive, nervous, endocrine, urinary, or reproductive systems. Inflammatory diseases include a broad array of disorders and conditions that are characterized by inflammation, ranging from autoimmune disease, atopic dermatitis, asthma, chronic obstructive pulmonary disease, inflammatory bowel disease, glomerulonephritis, hepatitis, reperfusion injury, transplant rejection, diabetes, cancer, Parkinson’s disease, multiple sclerosis, to depression. Epigenetic mechanisms play crucial roles in many biological processes by regulating transcriptional activation or repression. Histone post-translational modifications have emerged as prospective therapeutic targets. Methylation of histone 3 at lysine 9 is one of the most highly conserved epigenetic marks that correlate well with gene silencing. The methylation status of H3K9 modulates immune cell differentiation and immune responses and therefore influences the outcome of cancer, infection, and other inflammatory diseases. Here, we review the high impact and innovate discoveries in this field, highlight the critical role of the H3K9 methylation/de-methylation in human inflammatory diseases, discuss potential new therapeutic strategies based on a better understanding of the biology of H3K9 methylation modifications.

Abbreviations: 2OG: 2-oxoglutarate; AOL: Amine oxidase-like; ChIP: Chromatin immunoprecipitation; CNS2: conserved noncoding sequence 2; COPD: Chronic obstructive pulmonary disease; CoREST: Corepressor of RE1 silencing transcription factor; CPP: Cell-permeant protein; CTLA4: Cytotoxic T-lymphocyte antigen 4; DCs: Dendritic cells; DN: Diabetic nephropathy; ESRD: End-stage renal disease; ETDB: SET domain bifurcated histone lysine methyltransferase; FAD: Flavin adenine dinucleotide; FEV1%: The percentage of forced expiratory volume in one second; FEV1/FVC: Forced expiratory volume in one second (FEV1)/Forced vital capacity (FVC) value; FOXP3: forkhead/winged helix transcription factor 3; GLP: G9a like protein; GZMB: Granzyme B; H3K27me3: Trimethylation of lysine 27 on histone H3; H3K4me3: Trimethylation of lysine 4 on histone H3; H3K9: Histone 3 Lysine 9; HG: Hyperglycemia; HDAC3: Histone deacetylase 3; HP1: Heterochromatin protein 1; I/R: Ischemia/Reperfusion; IBD: Inflammatory bowel disease; IFN-: Interferon-; IFNG: Interferon Gamma; IL-2: Interleukin-2; ILC2s: Group 2 innate lymphoid cells; JMJD: Jumonji domain-containing protein; iTreg: inducible Treg; KDM: Lysine-specific demethylase; LPS: Lipopolysaccharide; LSD: Lys-specific demethylase; MCP-1: Monocyte chemoattractant protein-1; MCSF: Macrophage colony-stimulating factor; MIP-1: Macrophage inflammatory protein-1; MS: Metabolic syndrome; NAFLD: Non-alcoholic fatty liver disease; NKRF: NF-kappaB repressing factor; NOR: Norisoboldine; NuRD: Nucleosome remodeling and deacetylase; OxLDL: Oxidized low-density lipoprotein; PBMCs: Peripheral blood monocytes; PHD: Plant homology domain; Poly I:C: Polyinosinic:polycytidylic acid; PPARγ: Peroxisome proliferator-activated receptor gamma; PTMs: Post-translational modifications; SUV3-9: Suppressor of variegation3-9; T1D: Type 1 diabetes; TLRs: Toll like receptors; TSDR: TGF-β sensitive region and Treg cell specific demethylated region; Treg: Regulatory T cell; VSMCs: Vascular smooth muscle cells.

炎症是免疫系统对有害刺激（如病原体、受损细胞、有毒化合物或辐射）作出反应的一种防御机制。这些刺激可能在呼吸系统、心血管系统、消化系统、神经系统、内分泌系统、泌尿系统或生殖系统中诱发炎症反应和潜在的组织损伤。炎症性疾病包括一系列以炎症为特征的疾病和病症，包括自身免疫性疾病、特应性皮炎、哮喘、慢性阻塞性肺病、炎症性肠病、肾小球肾炎、肝炎、再灌注损伤、移植排斥、糖尿病、癌症、帕金森氏症疾病、多发性硬化症、抑郁症。表观遗传机制通过调节转录激活或抑制在许多生物过程中发挥着至关重要的作用。组蛋白翻译后修饰已成为前瞻性治疗靶点。组蛋白 3 在赖氨酸 9 处的甲基化是高度保守的表观遗传标记之一，与基因沉默密切相关。H3K9 的甲基化状态调节免疫细胞分化和免疫反应，因此影响癌症、感染和其他炎症疾病的结果。在这里，我们回顾了该领域的重大影响和创新发现，强调了 H3K9 甲基化/去甲基化在人类炎症性疾病中的关键作用，基于对 H3K9 甲基化修饰生物学的更好理解，讨论了潜在的新治疗策略。组蛋白 3 在赖氨酸 9 处的甲基化是高度保守的表观遗传标记之一，与基因沉默密切相关。H3K9 的甲基化状态调节免疫细胞分化和免疫反应，因此影响癌症、感染和其他炎症疾病的结果。在这里，我们回顾了该领域的重大影响和创新发现，强调了 H3K9 甲基化/去甲基化在人类炎症性疾病中的关键作用，基于对 H3K9 甲基化修饰生物学的更好理解，讨论了潜在的新治疗策略。组蛋白 3 在赖氨酸 9 处的甲基化是高度保守的表观遗传标记之一，与基因沉默密切相关。H3K9 的甲基化状态调节免疫细胞分化和免疫反应，因此影响癌症、感染和其他炎症疾病的结果。在这里，我们回顾了该领域的重大影响和创新发现，强调了 H3K9 甲基化/去甲基化在人类炎症性疾病中的关键作用，基于对 H3K9 甲基化修饰生物学的更好理解，讨论了潜在的新治疗策略。

缩写：2OG：2-氧戊二酸；AOL：胺氧化酶样；ChIP：染色质免疫沉淀；CNS2：保守的非编码序列2；COPD：慢性阻塞性肺病；CoREST：RE1沉默转录因子的Corepressor；CPP：细胞渗透蛋白；CTLA4：细胞毒性 T 淋巴细胞抗原 4；DCs：树突状细胞；DN：糖尿病肾病；ESRD：终末期肾病；ETDB：SET域分叉组蛋白赖氨酸甲基转移酶；FAD：黄素腺嘌呤二核苷酸；FEV1%：一秒用力呼气量的百分比；FEV1/FVC：一秒用力呼气量（FEV1）/用力肺活量（FVC）值；FOXP3：叉头/翼状螺旋转录因子3；GLP：G9a 样蛋白；GZMB：颗粒酶B；H3K27me3：组蛋白 H3 上赖氨酸 27 的三甲基化；H3K4me3：组蛋白 H3 上赖氨酸 4 的三甲基化；H3K9：组蛋白 3 赖氨酸 9；汞：高血糖症; HDAC3：组蛋白去乙酰化酶 3；HP1：异染色质蛋白 1；I/R：缺血/再灌注；IBD：炎症性肠病；IFN-：干扰素-；IFNG：γ干扰素；IL-2：白细胞介素-2；ILC2s：第 2 组先天淋巴细胞；JMJD：含有 Jumonji 结构域的蛋白质；iTreg：诱导型Treg；KDM：赖氨酸特异性脱甲基酶；LPS：脂多糖；LSD：赖氨酸特异性脱甲基酶；MCP-1：单核细胞趋化蛋白-1；MCSF：巨噬细胞集落刺激因子；MIP-1：巨噬细胞炎症蛋白-1；MS：代谢综合征；NAFLD：非酒精性脂肪肝；NKRF：NF-kappaB 抑制因子；NOR：去甲酚定；NuRD：核小体重塑和去乙酰化酶；OxLDL：氧化低密度脂蛋白；PBMC：外周血单核细胞；PHD：植物同源域；Poly I:C：聚肌苷酸：聚胞苷酸；PPARγ：过氧化物酶体增殖物激活受体 γ; PTM：翻译后修饰；SUV3-9：杂色抑制器3-9；T1D：1 型糖尿病；TLRs：Toll 样受体；TSDR：TGF-β敏感区和Treg细胞特异性去甲基化区；Treg：调节性T细胞；VSMCs：血管平滑肌细胞。