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
However, whether ClC-7 directly determines lysosomal acidity remains controversial.；Prospective studies should also determine whether BALF and blood measurements identify the same or distinct lysosomal phenotypes.；These phases are not mutually exclusive, and human studies are needed to determine whether measurable lysosomal phenotypes define clinically useful temporal or biological subgroups.8.3Hypotheses and open questionsSeveral mechanisms are retained because they generate specific, testable questions rather than because they are established in septic lung injury.
方法
A recent meta-analysis estimated that ARDS develops in 34.0% of patients with sepsis (95% confidence interval, 29.0%–39.3%) (Li et al., 2026), and alveolar–capillary barrier failure remains a central pathological feature (Ma et al., 2025; Chan et al., 2025).；We propose that disruption of these layers can create a candidate, context-dependent signal-amplifying hub, not a universal initiating lesion.；(B) Cell-specific consequences include defective macrophage pathogen clearance, altered epithelial lysosome-related organelle function, endothelial barrier-repair failure, and impaired fibroblast matrix turnover, collectively contributing to sepsis-associated lung injury.
核心结论
(B) Cell-specific consequences include defective macrophage pathogen clearance, altered epithelial lysosome-related organelle function, endothelial barrier-repair failure, and impaired fibroblast matrix turnover, collectively contributing to sepsis-associated lung injury.；(Liu Q. et al., 2026) further demonstrated across yeast and human cell systems that protons generated by the mitochondrial electron transport chain can support vacuolar or lysosomal acidification through interorganelle contacts.；Collectively, these findings suggest that changes in lysosomal pH may reflect not only alterations in V-ATPase activity and counterion conductance but also changes in mitochondria–lysosome contact dynamics and mitochondrial proton availability.
局限
Because the original narrative-review search log was not prospectively archived, a formal PRISMA study-flow count cannot be reconstructed reliably; this limitation is stated explicitly in Section 8.5.；Full study-level evidence and limitations are provided in Supplementary Table S1.3Lysosomal pH regulation in infection-relevant lung cells3.1V-ATPase as an acidification and signaling platformLysosomes are the principal acidic organelles for intracellular degradation and recycling, and lysosomal hydrolases generally require V-ATPase-dependent luminal acidification (Mindell, 2012; Suzuki et al., 2023).；However, whether ClC-7 directly determines lysosomal acidity remains controversial.
对本项目的价值
中高价值：属「营养感知—自噬—蛋白稳态轴」方向；mTOR / 自噬 / 蛋白质稳态栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.4/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 48,770 字符，题名指纹 1.0，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：溶酶体 pH 失调作为脓毒症相关肺损伤的候选信号放大枢纽
- 英文标题：Lysosomal pH dysregulation as a candidate signal-amplifying hub in sepsis-associated lung injury.
- 期刊与标识：Frontiers in cellular and infection microbiology · PMID 42978958 · DOI 10.3389/fcimb.2026.1953667 · PMC PMC13728857