Navarro-Lérida Inmaculada, Aragay Anna M, Asensio Alejandro, Ribas Catalina
Molecular Biology Department and Center of Molecular Biology "Severo Ochoa", CSIC-UAM, 28049 Madrid, Spain.
Health Research Institute "La Princesa", 28006 Madrid, Spain.
Antioxidants (Basel). 2022 Aug 18;11(8):1599. doi: 10.3390/antiox11081599.
All processes in human physiology relies on homeostatic mechanisms which require the activation of specific control circuits to adapt the changes imposed by external stimuli. One of the critical modulators of homeostatic balance is autophagy, a catabolic process that is responsible of the destruction of long-lived proteins and organelles through a lysosome degradative pathway. Identification of the mechanism underlying autophagic flux is considered of great importance as both protective and detrimental functions are linked with deregulated autophagy. At the mechanistic and regulatory levels, autophagy is activated in response to diverse stress conditions (food deprivation, hyperthermia and hypoxia), even a novel perspective highlight the potential role of physical forces in autophagy modulation. To understand the crosstalk between all these controlling mechanisms could give us new clues about the specific contribution of autophagy in a wide range of diseases including vascular disorders, inflammation and cancer. Of note, any homeostatic control critically depends in at least two additional and poorly studied interdependent components: a receptor and its downstream effectors. Addressing the selective receptors involved in autophagy regulation is an open question and represents a new area of research in this field. G-protein coupled receptors (GPCRs) represent one of the largest and druggable targets membrane receptor protein superfamily. By exerting their action through G proteins, GPCRs play fundamental roles in the control of cellular homeostasis. Novel studies have shown Gαq, a subunit of heterotrimeric G proteins, as a core modulator of mTORC1 and autophagy, suggesting a fundamental contribution of Gαq-coupled GPCRs mechanisms in the control of this homeostatic feedback loop. To address how GPCR-G proteins machinery integrates the response to different stresses including oxidative conditions and mechanical stimuli, could provide deeper insight into new signaling pathways and open potential and novel therapeutic strategies in the modulation of different pathological conditions.
人体生理学中的所有过程都依赖于稳态机制,这些机制需要激活特定的控制回路来适应外部刺激所带来的变化。自噬是稳态平衡的关键调节因子之一,它是一种分解代谢过程,通过溶酶体降解途径负责破坏长寿蛋白和细胞器。由于自噬通量的失调既与保护功能有关,也与有害功能有关,因此确定自噬通量背后的机制被认为非常重要。在机制和调节层面,自噬会响应多种应激条件(食物剥夺、高温和缺氧)而被激活,甚至一种新的观点强调了物理力在自噬调节中的潜在作用。了解所有这些控制机制之间的相互作用,可能会为我们提供关于自噬在包括血管疾病、炎症和癌症在内的多种疾病中的具体作用的新线索。值得注意的是,任何稳态控制都严重依赖于至少另外两个研究较少的相互依赖的组成部分:一个受体及其下游效应器。确定参与自噬调节的选择性受体是一个悬而未决的问题,也是该领域的一个新研究领域。G蛋白偶联受体(GPCRs)是最大的可成药膜受体蛋白超家族之一。通过G蛋白发挥作用,GPCRs在细胞稳态控制中发挥着基本作用。新的研究表明,异源三聚体G蛋白的一个亚基Gαq是mTORC1和自噬的核心调节因子,这表明Gαq偶联的GPCRs机制在控制这种稳态反馈回路中具有重要作用。研究GPCR-G蛋白机制如何整合对包括氧化条件和机械刺激在内的不同应激的反应,可能会更深入地了解新的信号通路,并为调节不同病理状况开辟潜在的新治疗策略。