该课题组人员发现过氧化物酶体通过接触介导的活性氧（ROS）转移在维持线粒体氧化还原稳态中起直接作用。研究组发现ACBD5和PTPIP51在过氧化物酶体和线粒体之间形成一种接触。这些接触的百分比在线粒体氧化应激期间增加，并通过将线粒体活性氧转移到过氧化物酶体管腔来帮助维持线粒体健康。他们的发现揭示了线粒体抗氧化防御的多细胞器层——暗示了过氧化物酶体促进线粒体健康的直接机制——并扩大了已知膜接触部位功能的范围。
据悉，线粒体氧化还原稳态的维持对细胞健康至关重要。线粒体拥有许多内在的抗氧化防御，但外在的非线粒体抗氧化机制的作用尚不清楚。
附：英文原文
Title: ROS transfer at peroxisome-mitochondria contact regulates mitochondrial redox
Author: Laura F. DiGiovanni, Prabhsimran K. Khroud, Ruth E. Carmichael, Tina A. Schrader, Shivneet K. Gill, Kyla Germain, Robert Y. Jomphe, Christoph Wiesinger, Maxime Boutry, Maki Kamoshita, Daniel Snider, Garret Stubbings, Rong Hua, Noel Garber, Christian Hacker, Andrew D. Rutenberg, Roman A. Melnyk, Johannes Berger, Michael Schrader, Brian Raught, Peter K. Kim
Issue&Volume: 2025-07-10
Abstract: Maintenance of mitochondrial redox homeostasis is of fundamental importance to cellular health. Mitochondria harbor a host of intrinsic antioxidant defenses, but the contribution of extrinsic, nonmitochondrial antioxidant mechanisms is less well understood. We found a direct role for peroxisomes in maintaining mitochondrial redox homeostasis through contact-mediated reactive oxygen species (ROS) transfer. We found that ACBD5 and PTPIP51 form a contact between peroxisomes and mitochondria. The percentage of these contacts increased during mitochondrial oxidative stress and helped to maintain mitochondrial health through the transfer of mitochondrial ROS to the peroxisome lumen. Our findings reveal a multiorganelle layer of mitochondrial antioxidant defense—suggesting a direct mechanism by which peroxisomes contribute to mitochondrial health—and broaden the scope of known membrane contact site functions.
DOI: adn2804
Source: https://www.science.org/doi/10.1126/science.adn2804