Apelin–APLNR pathway across development, inflammation, and vascular remodeling: an endothelial perspective

Engineering notes

Key topics: autonomous driving. See the paper for implementation details and experimental results.

Chinese explanation / 中文解读

中文解读待补充：本站会优先为端到端自动驾驶、BEV感知、3D目标检测、轨迹预测、路径规划、LiDAR感知等高价值论文补充中文说明。

Original abstract

Abstract The apelinergic system, composed of the ligands Apelin and Elabela and their shared receptor APLNR, has key functions in vascular development and endothelial homeostasis. Originally identified as an orphan G protein-coupled receptor, APLNR is now recognized as a receptor highly enriched in endothelial cells across organs, where it integrates developmental cues, mechanical forces, hypoxia, and inflammatory signals. Apelin and Elabela guide angiogenic patterning during cardiac, pulmonary, and retinal development, and in adulthood they support endothelial nitric oxide production, vascular stability, and tissue adaptation to stress. Pathological conditions expose the dependence of endothelial integrity on this pathway. Reduced Apelin availability or altered APLNR expression contributes to hypertension, cardiac remodeling, pulmonary vascular injury, and immune-driven inflammation. Conversely, restoring apelinergic signaling improves endothelial barrier function, limits leukocyte recruitment, and mitigates fibrotic and ischemic damage, including in experimental models of autoimmune encephalomyelitis and acute lung injury. Therapeutic interest in this pathway has increased with the development of stabilized Apelin analogs and small-molecule APLNR agonists that have longer half-lives than native peptides. Together, emerging evidence positions the Apelin–APLNR axis as a context-dependent regulator of endothelial function and a promising therapeutic target in cardiovascular, pulmonary, and inflammatory diseases.

Links and sources

• PDF from original source

Comments