bims-lycede Biomed News
on Lysosome-dependent cell death
Issue of 2026–08–23
two papers selected by
Sofía Peralta, Universidad Nacional de Cuyo



  1. Anal Chem. 2026 Aug 18. 98(32): 23762-23773
      Mitochondrial or lysosomal damage is the initial step of apoptosis, and detecting their damaging sequences is crucial for understanding programmed cell death and related diseases. However, fluorescent probes capable of reporting their damaging order are rarely reported, owing to the deficiency of valid strategies. Herein, by rationally modifying targeting groups and employing a side-chain regulation strategy, a probe Trav was designed to detect the temporal order of lysosomal and mitochondrial damage. Trav targeted both mitochondria and lysosomes in living cells and distinguished them from each other with different fluorescence colors. Upon mitochondrial damage, Trav translocated to lysosomes, accompanied by a fluorescence color change. Subsequently, after lysosomal damage, Trav was relocated to the nucleus and emitted a third color. Similarly, if lysosomal damage occurs first, Trav migrates to mitochondria, which relocated into the nucleus after subsequent mitochondrial damage. Thus, Trav enabled reporting the damaging order of mitochondria and lysosomes through subcellular translocation and fluorescence color changes. Using Trav, we successfully revealed that in hyperthermia-induced injury lysosomal damage preceded mitochondrial damage, and this process was associated with increased levels of reactive oxygen species. Reducing agents, such as cysteine, can inhibit the injury. Trav holds promise as a valuable molecular tool for advancing research in related biomedical fields.
    DOI:  https://doi.org/10.1021/acs.analchem.6c03203
  2. Arch Razi Inst. 2025 Nov;80(6): 1379-1392
      Autophagy is an evolutionarily conserved, lysosome-dependent, intracellular degradation process that is essential for maintaining cellular homeostasis and adaptation to cellular stresses in eukaryotic cells. Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) that cause damage to lipids, proteins, and DNA. Oxidative stress has been linked to a myriad of pathologies. Autophagy can be involved in various biological processes such as programmed cell death, stress responses, removal of damaged organelles, and growth. The role of autophagy has been identified as a critical mediator in the pathological response to redox signaling. Autophagy is considered a main sensor of redox signaling. ROS are highly reactive molecules produced as byproducts of cellular metabolism, mainly by mitochondria. Mitochondrial ROS (mROS) can be beneficial or harmful to cells depending on their concentration and location. mROS at low physiological concentrations act as redox messengers in intracellular signaling, while overproduction of mROS causes oxidative damage to cellular components and ultimately leads to cell death. Hence, the balance of stress adaptation associated with autophagy and cell death is important for understanding pathogenesis related to redox signaling. Autophagy is an integral biological process critical for cellular and organismal homeostasis. It allows spatial reorganization and energy supply to cells through the regular destruction machinery of unnecessary or inefficient components. In this review, we focus on the basic mechanisms and functions of autophagy in response to oxidative stress and redox signaling in pathology.
    Keywords:   Autophagy; Homeostasis; Oxidative stress; mROS
    DOI:  https://doi.org/10.32598/ARI.80.6.3391