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
By reframing PTMs as dynamic and interacting regulatory systems rather than isolated molecular events, we aim to provide a conceptual framework for more selective vascular interventions that may complement existing anti‐inflammatory and lipid‐lowering approaches.2Overview of Atherosclerosis PathogenesisAS, a chronic vasculopathy of large and medium‐sized arteries, is characterized by inflammatory reactions [55, 56, 57], deranged lipid metabolism [58, 59], and vascular plaque formation [60, 61].；Whether HDAC9‐dependent deacetylation overlaps functionally with H3K27me3 deposition by modifiers such as EZH2 remains untested in vascular tissue.；Whether protective immune surveillance is preserved over longer exposures has not been tested.
方法
Section 7 applies this framework systematically, distinguishing cross‐talk demonstrated at residue resolution from cross‐talk currently inferred from pathway convergence.In this review, we integrate current mechanistic knowledge across PTM classes, emphasize their interconnected and context‐dependent roles in vascular cells, and summarize emerging translational strategies for targeting complementary PTM pathways in atherosclerosis.；By reframing PTMs as dynamic and interacting regulatory systems rather than isolated molecular events, we aim to provide a conceptual framework for more selective vascular interventions that may complement existing anti‐inflammatory and lipid‐lowering approaches.2Overview of Atherosclerosis PathogenesisAS, a chronic vasculopathy of large and medium‐sized arteries, is characterized by inflammatory reactions [55, 56, 57], deranged lipid metabolism [58, 59], and vascular plaque formation [60, 61].；Endothelium‐specific PKN1 loss or an S31 phospho‐deficient H3.3 mutant reduces endothelial inflammation.HUAECs; endothelial PKN1‐knockout and H3.3 S31A micePro‐atherogenicE3‡[22]Phosphorylation (GRK2)Vinculin Ser721VCLS721p locks vinculin in an inactive, closed conformation, disrupting the VE‐cadherin/catenin complex and increasing permeability.
核心结论
Section 7 applies this framework systematically, distinguishing cross‐talk demonstrated at residue resolution from cross‐talk currently inferred from pathway convergence.In this review, we integrate current mechanistic knowledge across PTM classes, emphasize their interconnected and context‐dependent roles in vascular cells, and summarize emerging translational strategies for targeting complementary PTM pathways in atherosclerosis.；In summary, AS arises from endothelial dysfunction and lipoprotein retention, progresses through chronic inflammation and maladaptive repair, and culminates in fibrous plaque formation with the risk of rupture and thrombosis, an interplay of immune activation, lipid metabolism, and vascular remodeling.；Demonstrated in acute lung injury models rather than atherosclerosis.Endothelial cells; murine acute lung injury modelsProtectiveE3/E4[124]Macrophages and myeloid cellsPhosphorylation (WEE1)NF‐κB p65 Ser536WEE1 binds p65 directly and phosphorylates Ser536, inducing inflammatory transcription and driving lesion growthMacrophages; Apoe−/− micePro‐atherogenicE3[32]Phosphorylation (site disrupted by knock‐in)LXRα Ser196Myeloid S196A substitution reprogrammed the macrophage transcriptome, inducing FoxM1 and plaque‐resident cell proliferation, and increasing efferocytosis.
局限
Convergence, however, is not the same as interaction, and the distinction is central to this review: cross‐talk between modifications is not a metaphor for shared pathway membership but a set of biochemical relationships that can be specified and, in principle, falsified, at the level of individual residues and enzymes [25, 26, 31].；The Wnt/β‐catenin–Runx2 osteogenic axis is mechanistically the sharpest node considered here, since smooth‐muscle‐restricted Ogt deletion attenuates phosphate‐induced mineralization and pharmacological Wnt activation restores it [19]; it is nonetheless confined to one cell type and one disease process, and is likewise unanchored in human tissue.One heavily represented family warrants explicit de‐prioritization.；MAPK cascades occupy a substantial share of the vascular PTM literature; however, they rank lowest on these criteria.
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 192,578 字符，题名指纹 0.69，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：血管细胞翻译后修饰串扰：动脉粥样硬化的分子机制与治疗意义
- 英文标题：Posttranslational Modification Cross-Talk in Vascular Cells: Molecular Mechanisms and Therapeutic Implications for Atherosclerosis.
- 期刊与标识：Cell biochemistry and function · PMID 42968629 · DOI 10.1002/cbf.70329 · PMC PMC13725273