将其结论的小标题和对应的总结句子找出，可得到以下信息：

结论一：Stroke induces long-term inflammatory changes in systemic monocytes/macrophages（中风引起全身单核/巨噬细胞的长期炎症变化）

总结句：Stroke chronically promotes the recruitment of circulating Ly6Chigh monocytes to the heart, which might further differentiate into tissue-resident macrophages. （中风慢性促进循环ly6high单核细胞向心脏募集，这些细胞可能进一步分化为组织内巨噬细胞。）

延伸的信息：中风会引起全身炎症反应，大概率会进一步影响其他器官（大概率是炎症反应主导的），此时看到Figure1图

Figure 1.  A-C

创新点的来源一：靶向中风后最有可能受炎症影响的器官（血液/肺/心脏/脾脏/肝脏），因为这些器官“have previously been associated with inflammatory consequences of brain injury in the acute phase.”

创新点的来源二：关注中风慢性期后的差异基因变化，即Figure 1C。“We found a large number of genes to still be differentially regulated at this late chronic time point after stroke, particularly within the population of monocytes/macrophages, while other cell populations, including neutrophils or dendritic cells, were less affected.”

结论二：Stroke results in chronic cardiac diastolic dysfunction. 中风导致慢性心脏舒张功能障碍

总结句：Cardiac fibrosis and ECM remodeling in both experimental mice and stroke patients, which was further associated with diastolic dysfunction after experimental stroke. 实验小鼠和脑卒中患者的心脏纤维化和ECM重塑，与实验性脑卒中后舒张功能障碍相关。

延伸的信息：1）中风后检测心脏功能（0到28天的收缩与舒张功能检测），发现慢性心脏舒张功能障碍；2）寻找导致舒张功能障碍的原因：纤维化/细胞外基质/肾功能障碍/心脏总体解剖改变/自主心脏神经的持续扰动无关等表型，仅看到中风后慢性期的心脏纤维化，与细胞外基质中胶原杂乱分布。

总结句：A hallmark of this secondary cardiac pathology after stroke is the increased recruitment and pro-inflammatory profile of cardiac monocytes/macrophages. 中风后继发性心脏病理的一个标志是心脏单核/巨噬细胞的募集增加和促炎特征。

创新点三：言之有理的下游实验（单细胞测序发现中风后慢性期通过全身炎症影响心脏，故心脏超声检测心脏/流式观察炎症细胞变化，且是否与心脏表型相关），从中发现新现象：中风后慢性期通过炎症反应影响心脏纤维化与细胞外基质，导致慢性舒张功能障碍。

结论三：Stroke promotes chronic monocyte recruitment into the heart. 中风促进慢性单核细胞募集进入心脏

结论四：BM cellularity and function are chronically altered after stroke. 中风后骨髓细胞结构和功能发生慢性改变

结论五：Stroke induces persistent innate immune memory. 中风诱发持久的先天免疫记忆

总结句：Myeloid function is not only stably altered after stroke but that these changes in the myeloid compartment are sufficient to drive secondary cardiac fibrosis. 髓系功能不仅在中风后稳定改变，而且髓系的这些改变足以驱动继发性心脏纤维化。

延伸信息：中风后的诱发全身炎症，并且到心脏中的心脏细胞从哪里来？——利用谱系示踪技术阐明这一问题

创新点四：回答细胞在“刺激”下“如何变”，并用最合适的实验“看到它的变”

结论六：Innate immune memory is mediated by early post-stroke IL-1β secretion中风后早期IL-1β分泌介导了先天免疫记忆

总结句：the critical role of IL-1β in inducing epigenetic changes leading to post-stroke-trained immunity. IL-1β在诱导中风后免疫的表观遗传变化中发挥关键作用。

延伸信息：1）免疫训练：先天免疫细胞对后续刺激的强烈反应，可用免疫细胞对细胞因子刺激（如LPS）的反应实验观察；2）免疫训练受到表观遗传调控

创新点五：落脚于“免疫训练”和“IL-1β”和”表观遗传”

结论七：IL-1β-driven innate immune memory mediates remote organ dysfunction after stroke. lL -1β驱动的先天免疫记忆介导脑卒中后远端器官功能障碍

总结句：the IL-1β-driven epigenetic changes leading to trained immunity can be causally involved in mediating the chronic cardiac fibrosis after stroke. IL -1β驱动的表观遗传变化导致的免疫训练可能与中风后慢性心脏纤维化有关。

延伸信息：前期实验数据导向，必须回答“是否lL -1β（表观遗传）驱动的免疫训练影响了中风后的慢性舒张功能障碍”

结论八：Blocking BM-to-heart trafficking of monocytes prevents post-stroke cardiac dysfunction阻断骨髓到心脏的单核细胞运输可预防脑卒中后心功能障碍

总结句：the therapeutic potential of blocking the BM-to-heart migration of pro-inflammatory programmed monocytes as a strategy to prevent secondary cardiac comorbidity following stroke阻断促炎程序性单核细胞向心脏迁移的治疗潜力，作为预防中风后继发性心脏合并症的策略

延伸信息：目前抗炎治疗为何疗效不佳？可能同时影响整个机体，例如导致感染风险增加，故更为精确的治疗手段似乎更为合适

创新点六：找到精准方向：阻断骨髓到心脏的炎症细胞募集；提供更精准的治疗方案（阻断炎症细胞迁移）

期待已久~

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