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Cardiac Fibroblastic Niches in Homeostasis and Inflammation.
Circulation Research ( IF 16.5 ) Pub Date : 2024-06-06 , DOI: 10.1161/circresaha.124.323892 Nadine Cadosch 1 , Cristina Gil-Cruz 1, 2 , Christian Perez-Shibayama 1 , Burkhard Ludewig 1, 2, 3
Circulation Research ( IF 16.5 ) Pub Date : 2024-06-06 , DOI: 10.1161/circresaha.124.323892 Nadine Cadosch 1 , Cristina Gil-Cruz 1, 2 , Christian Perez-Shibayama 1 , Burkhard Ludewig 1, 2, 3
Affiliation
Fibroblasts are essential for building and maintaining the structural integrity of all organs. Moreover, fibroblasts can acquire an inflammatory phenotype to accommodate immune cells in specific niches and to provide migration, differentiation, and growth factors. In the heart, balancing of fibroblast activity is critical for cardiac homeostasis and optimal organ function during inflammation. Fibroblasts sustain cardiac homeostasis by generating local niche environments that support housekeeping functions and by actively engaging in intercellular cross talk. During inflammatory perturbations, cardiac fibroblasts rapidly switch to an inflammatory state and actively communicate with infiltrating immune cells to orchestrate immune cell migration and activity. Here, we summarize the current knowledge on the molecular landscape of cardiac fibroblasts, focusing on their dual role in promoting tissue homeostasis and modulating immune cell-cardiomyocyte interaction. In addition, we discuss potential future avenues for manipulating cardiac fibroblast activity during myocardial inflammation.
中文翻译:
心脏成纤维细胞在稳态和炎症中的地位。
成纤维细胞对于构建和维持所有器官的结构完整性至关重要。此外,成纤维细胞可以获得炎症表型,以将免疫细胞容纳在特定的环境中,并提供迁移、分化和生长因子。在心脏中,成纤维细胞活性的平衡对于炎症期间心脏稳态和最佳器官功能至关重要。成纤维细胞通过产生支持管家功能的局部利基环境并积极参与细胞间串扰来维持心脏稳态。在炎症扰动期间,心脏成纤维细胞迅速切换到炎症状态,并积极与浸润的免疫细胞沟通,协调免疫细胞的迁移和活动。在这里,我们总结了目前关于心脏成纤维细胞分子景观的知识,重点关注它们在促进组织稳态和调节免疫细胞-心肌细胞相互作用方面的双重作用。此外,我们讨论了在心肌炎症期间操纵心脏成纤维细胞活性的潜在未来途径。
更新日期:2024-06-06
中文翻译:
心脏成纤维细胞在稳态和炎症中的地位。
成纤维细胞对于构建和维持所有器官的结构完整性至关重要。此外,成纤维细胞可以获得炎症表型,以将免疫细胞容纳在特定的环境中,并提供迁移、分化和生长因子。在心脏中,成纤维细胞活性的平衡对于炎症期间心脏稳态和最佳器官功能至关重要。成纤维细胞通过产生支持管家功能的局部利基环境并积极参与细胞间串扰来维持心脏稳态。在炎症扰动期间,心脏成纤维细胞迅速切换到炎症状态,并积极与浸润的免疫细胞沟通,协调免疫细胞的迁移和活动。在这里,我们总结了目前关于心脏成纤维细胞分子景观的知识,重点关注它们在促进组织稳态和调节免疫细胞-心肌细胞相互作用方面的双重作用。此外,我们讨论了在心肌炎症期间操纵心脏成纤维细胞活性的潜在未来途径。