Biosensors reveal subcellular redox status in live cells

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Journal of molecular and cellular cardiology Pub Date : 2026-03-01 Epub Date: 2025-12-20 DOI:10.1016/j.yjmcc.2025.12.009

Haoqi Li , Huimin Li , Yufan Chao , Yaozhao Li , Zijie Cheng , Yuqing Li , Yun Yin , Tao Chen , Xin Dong , Dan Wu , Qingxun Hu

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Abstract

Redox homeostasis is crucial for cellular function and signaling, with its disruption linked to various diseases. Given the compartment-specific nature of redox regulation, we employed highly responsive genetically encoded fluorescent sensors, including Hyper7, iNap, and roGFP2, to achieve real-time in situ tracking of the redox dynamics of H₂O₂, NADPH and GSH in the cytoplasm and mitochondria. It revealed that glycolysis and oxidative phosphorylation differentially modulate redox metabolites across subcellular domains, demonstrating metabolic pathway-specific regulation of redox equilibrium. Pathological modeling (cardiac hypertrophy, ischemia-reperfusion and cuproptosis) characterized mitochondrial redox systems exhibit superior stress-responsive regulation versus cytoplasmic counterparts, displaying enhanced dynamic responses during injury progression. These results suggest that precise subcellular redox mapping delivers critical insights into dynamic signal transduction mechanisms and proposes targeted therapeutic avenues for redox-associated pathologies through compartment-specific interventions.

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生物传感器揭示活细胞的亚细胞氧化还原状态

氧化还原稳态对细胞功能和信号传导至关重要，其破坏与各种疾病有关。考虑到氧化还原调控的室特异性，我们采用了高响应的遗传编码荧光传感器，包括Hyper7、iNap和roGFP2，来实现对细胞质和线粒体中H2O2、NADPH和GSH氧化还原动力学的实时原位跟踪。研究表明，糖酵解和氧化磷酸化对氧化还原代谢产物在亚细胞结构域的差异调节，证明了氧化还原平衡的代谢途径特异性调节。病理模型（心脏肥厚、缺血-再灌注和铜变）表征线粒体氧化还原系统表现出优于细胞质对应系统的应激反应调节，在损伤进展过程中表现出增强的动态反应。这些结果表明，精确的亚细胞氧化还原图谱为动态信号转导机制提供了重要见解，并通过区室特异性干预为氧化还原相关病理提供了靶向治疗途径。

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来源期刊

Journal of molecular and cellular cardiology 医学-细胞生物学

CiteScore

10.70

自引率

0.00%

发文量

171

审稿时长

42 days

期刊介绍： The Journal of Molecular and Cellular Cardiology publishes work advancing knowledge of the mechanisms responsible for both normal and diseased cardiovascular function. To this end papers are published in all relevant areas. These include (but are not limited to): structural biology; genetics; proteomics; morphology; stem cells; molecular biology; metabolism; biophysics; bioengineering; computational modeling and systems analysis; electrophysiology; pharmacology and physiology. Papers are encouraged with both basic and translational approaches. The journal is directed not only to basic scientists but also to clinical cardiologists who wish to follow the rapidly advancing frontiers of basic knowledge of the heart and circulation.