Cooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.
Cooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.
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DOI：
10.1016/j.mbplus.2021.100089
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发表时间：
2021-12
影响因子：
--
通讯作者：
Thompson LM
中科院分区：
文献类型：
--
作者：
Hernandez SJ;Fote G;Reyes-Ortiz AM;Steffan JS;Thompson LM
黏附和自噬相互协同调节。这些过程在保护和退化的交叉点上发挥作用。了解重叠的分子功能可能会揭示治疗策略。由细胞外基质(ECM)引导的细胞黏附连接和通过自噬维持细胞内平衡似乎是分子上相互交织、相互调节的不同功能。这是大脑中的一个新兴领域，黏附和自噬之间的相互作用在神经保护和神经退化的交叉点发挥作用。细胞外基质和黏附蛋白调节自噬反应，以直接清除蛋白质，并指导在大脑疾病中出错的再生程序。同时，自噬通量调节黏附动力学，调节神经退行性疾病引起的神经突起生长和突触可塑性以及功能障碍。这篇综述强调了健康和疾病期间大脑中细胞黏附和自噬之间的合作交换。由于黏附和自噬之间的机制联盟已经被用于治疗转移性疾病，了解指导黏附和自噬之间相互作用的重叠分子功能可能会发现纠正或补偿神经退行性变的治疗策略。
Adhesion and autophagy synergistically regulate one another. These processes function at the intersection of protection and degeneration. Understanding overlapping molecular functions may uncover therapeutic strategies. Cellular adhesive connections directed by the extracellular matrix (ECM) and maintenance of cellular homeostasis by autophagy are seemingly disparate functions that are molecularly intertwined, each regulating the other. This is an emerging field in the brain where the interplay between adhesion and autophagy functions at the intersection of neuroprotection and neurodegeneration. The ECM and adhesion proteins regulate autophagic responses to direct protein clearance and guide regenerative programs that go awry in brain disorders. Concomitantly, autophagic flux acts to regulate adhesion dynamics to mediate neurite outgrowth and synaptic plasticity with functional disruption contributed by neurodegenerative disease. This review highlights the cooperative exchange between cellular adhesion and autophagy in the brain during health and disease. As the mechanistic alliance between adhesion and autophagy has been leveraged therapeutically for metastatic disease, understanding overlapping molecular functions that direct the interplay between adhesion and autophagy might uncover therapeutic strategies to correct or compensate for neurodegeneration.