ReviewOxidative medicine and cellular longevity2019
Mitochondrial Entry of Cytotoxic Proteases: A New Insight into the Granzyme B Cell Death Pathway.
Review in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
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- Apoptosis as an evolutionary battleground: pathogen pressure and the shaping of programmed cell death pathways.Frontiers in cell and developmental biology · 2026Review
- The application and prospect of granzyme B-targeted PET imaging in cancer immunotherapy.Journal of translational medicine · 2025Review
- The evolution of integrated magnetic hyperthermia and chemodynamic therapy for combating cancer: a comprehensive viewpoint.Nanoscale advances · 2025Review
- BH3 mimetics augment cytotoxic T cell killing of acute myeloid leukemia via mitochondrial apoptotic mechanism.Cell death discovery · 2025Article
- A new weapon: the application of tumor vaccines based on extracellular exosomal heat shock proteins in immunotherapy.Frontiers in immunology · 2025Review
- The antitumor effect of extracellular vesicles derived from cytokine-activated CD8+ T cells.Journal of leukocyte biology · 2024Article
- Modulating Nitric Oxide: Implications for Cytotoxicity and Cytoprotection.Antioxidants (Basel, Switzerland) · 2024Review
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
- Follicular fluid meiosis-activating sterol prevents porcine ovarian granulosa cells from hypoxia-induced apoptosis via inhibiting STAT4 expression.Journal of animal science · 2024Article
- Granzymes in health and diseases: the good, the bad and the ugly.Frontiers in immunology · 2024Review
- Mechanically active integrins target lytic secretion at the immune synapse to facilitate cellular cytotoxicity.Nature communications · 2022Article
- Immune-mediated neurodegenerative trait provoked by multimodal derepression of long-interspersed nuclear element-1.iScience · 2022Article
- Effective natural inhibitors targeting granzyme B in rheumatoid arthritis by computational study.Frontiers in medicine · 2022Article
- Escaping Death: How Cancer Cells and Infected Cells Resist Cell-Mediated Cytotoxicity.Frontiers in immunology · 2022Review
- Cytotoxic Action of Palladium-Based Compound on Prostate Stem Cells, Primary Prostate Epithelial Cells, Prostate Epithelial Cells, and Prostate Cell Lines.Journal of healthcare engineering · 2022Article
- Human NK cells: From development to effector functions.Innate immunity · 2021Review
- Switching from Apoptosis to Pyroptosis: Gasdermin-Elicited Inflammation and Antitumor Immunity.International journal of molecular sciences · 2021Review
- Cytotoxic T cells response with decreased CD4/CD8 ratio during mammary tumors inhibition in rats induced by non-contact electric fields.F1000Research · 2021Article
- MICA-G129R: A bifunctional fusion protein increases PRLR-positive breast cancer cell death in co-culture with natural killer cells.PloS one · 2021Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondria represent an integration and amplification hub for various death pathways including that mediated by granzyme B (GB), a granule enzyme expressed by cytotoxic lymphocytes. GB activates the proapoptotic B cell CLL/lymphoma 2 (Bcl-2) family member BH3-interacting domain death agonist (BID) to switch on the intrinsic mitochondrial death pathway, leading to Bcl-2-associated X protein (Bax)/Bcl-2 homologous antagonist/killer- (Bak-) dependent mitochondrial outer membrane permeabilization (MOMP), the dissipation of mitochondrial transmembrane potential (ΔΨm), and the production of reactive oxygen species (ROS). GB can also induce mitochondrial damage in the absence of BID, Bax, and Bak, critical for MOMP, indicating that GB targets the mitochondria in other ways. Interestingly, granzyme A (GA), GB, and caspase 3 can all directly target the mitochondrial respiratory chain complex I for ROS-dependent cell death. Studies of ROS biogenesis have revealed that GB must enter the mitochondria for ROS production, making the mitochondrial entry of cytotoxic proteases (MECP) an unexpected critical step in the granzyme death pathway. MECP requires an intact ΔΨm and is mediated though Sam50 and Tim22 channels in a mtHSP70-dependent manner. Preventing MECP severely compromises GB cytotoxicity. In this review, we provide a brief overview of the canonical mitochondrial death pathway in order to put into perspective this new insight into the GB action on the mitochondria to trigger ROS-dependent cell death.
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