时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
Increased matrix stiffness and disturbed flow can modulate macrophage inflammatory polarization as well as phagocytic or pro-calcific functions through mechanosensitive pathways, although whether similar stiffness-dependent reprogramming occurs within stenotic valve microenvironments has not been directly examined (16, 50, 89).Nevertheless, macrophage phenotypes in CAVD are unlikely to conform to a binary M1/M2 classification.；Further mechanistic studies are needed to validate whether mast cell localization, degranulation activity, and protease function directly regulate fibro-calcific remodeling in CAVD.4.5NeutrophilsNeutrophils are rapid responders to tissue injury, yet direct evidence supporting their pathogenic role in CAVD remains more limited than for macrophages or T cells.；Further studies are needed to determine whether specific CD8+ T cell states or effector pathways represent therapeutically actionable targets in CAVD.5.3B cellsB cells are rarely detected in healthy aortic valves but accumulate selectively in calcified lesions, particularly on the aortic leaflet surface and around neovessels (107).
方法
As leaflet stiffness and valve obstruction worsen, patients are at risk of heart failure, syncope, and increased mortality (3, 4).；Given ongoing population aging, the clinical and socioeconomic burden imposed by CAVD is expected to rise further (1, 2, 8).Once largely regarded as a passive consequence of aging, CAVD is now recognized as an active, cell-mediated disease involving mechanical stress, endothelial dysfunction, lipid retention, chronic inflammation, ECM remodeling, and multicellular crosstalk (5–7).；We further discuss sex-related differences, limitations of experimental models, therapeutic timing, patient stratification, and emerging strategies for targeted intervention.
核心结论
Histological and immunohistochemical analyses of valves previously categorized as degenerative AS first demonstrated lipid accumulation and immune cell infiltration within early-stage lesions (12).；These findings form the framework for the current emphasis on immune–stromal crosstalk, which is discussed in greater mechanistic detail in Section 5-6.；Collectively, osteogenic remodeling and mineral deposition are prominent features of advanced fibrocalcific CAVD, although inflammatory, fibrotic, and mineralization-related processes can overlap substantially across disease stages (9, 10, 39–41).
局限
These therapeutic limitations have increased interest in defining the immune and stromal mechanisms that operate during potentially modifiable stages of CAVD and in identifying interventions that may act before advanced fibrocalcific remodeling becomes established (21–24).Previous reviews have summarized inflammatory pathways or individual immune-cell populations implicated in CAVD.；However, important questions remain regarding how immune-cell heterogeneity interacts with the changing valvular microenvironment across disease stages and how these interactions influence the timing and feasibility of therapeutic intervention.；We further discuss sex-related differences, limitations of experimental models, therapeutic timing, patient stratification, and emerging strategies for targeted intervention.
对本项目的价值
中高价值：属「干细胞 / 部分重编程与再生」方向；干细胞 / 再生 / 重编程栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.1/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 77,432 字符，题名指纹 0.73，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：钙化性主动脉瓣病的免疫驱动重塑：机制与免疫治疗机会
- 英文标题：Immune-driven remodeling in calcific aortic valve disease: mechanisms and immunotherapeutic opportunities.
- 期刊与标识：Frontiers in immunology · PMID 42973842 · DOI 10.3389/fimmu.2026.1906690 · PMC PMC13725199