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神经元G蛋白偶联受体OCTR-1调节对温暖和寒冷温度的寿命反应。

The neuronal GPCR OCTR-1 modulates longevity responses to both warm and cold temperatures.

作者信息

Wibisono Shawndra, Wibisono Phillip, Chen Chia-Hui, Sun Jingru, Liu Yiyong

机构信息

Department of Translational Medicine and Physiology, Elson S. Floyd College of Medicine, Washington State University, Spokane, WA, USA.

Genomics Core, Washington State University, Spokane, WA, USA.

出版信息

iScience. 2025 Mar 22;28(4):112279. doi: 10.1016/j.isci.2025.112279. eCollection 2025 Apr 18.

Abstract

Many animal species live longer in cold climates than in warm climates, which was traditionally explained using the rate of living theory, i.e., higher temperatures increase chemical reaction rates, thus speeding up the aging process. However, recent studies have identified specific molecules and cells that are involved in longevity responses to temperature, indicating that such responses are not simply thermodynamic but are regulated processes. Here, we report that lacking the neuronal G protein-coupled receptor OCTR-1 have extended lifespans at a warm temperature but shortened lifespans at a cold temperature, demonstrating that OCTR-1 modulates temperature-induced longevity responses. These responses are regulated by the OCTR-1-expressing, chemosensory ASH neurons. Furthermore, the OCTR-1 pathway controls such responses to warm and cold temperatures by regulating the expressions of immune response genes and the intestinal transcriptional factor ELT-2, respectively. Overall, our study provides cellular and molecular insights into the relationship between temperature and longevity.

摘要

许多动物物种在寒冷气候中比在温暖气候中寿命更长,传统上用生命速率理论来解释这一现象,即较高的温度会提高化学反应速率,从而加速衰老过程。然而,最近的研究已经确定了参与对温度的长寿反应的特定分子和细胞,这表明这种反应并非简单的热力学过程,而是受调控的过程。在此,我们报告称,缺乏神经元G蛋白偶联受体OCTR-1的动物在温暖温度下寿命延长,但在寒冷温度下寿命缩短,这表明OCTR-1调节温度诱导的长寿反应。这些反应由表达OCTR-1的化学感应ASH神经元调节。此外,OCTR-1途径分别通过调节免疫反应基因和肠道转录因子ELT-2的表达来控制对温暖和寒冷温度的这种反应。总体而言,我们的研究为温度与寿命之间的关系提供了细胞和分子层面的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/449c/12013480/e1e24a27d1b7/gr1.jpg

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