ArticleBiochemistry and biophysics reports2022
The antimicrobial peptide LL-37 triggers release of apoptosis-inducing factor and shows direct effects on mitochondria.
Article in Biochemistry and biophysics reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Apoptosis Modulation by LL-37: From Mitochondrial Cell Death to Prosurvival Signaling.International journal of molecular sciences · 2026Review
- Peptide-Based Strategies AgainstPharmaceuticals (Basel, Switzerland) · 2025Review
- D-M159 Synergistically Induces Apoptosis in HeLa Cells Through Endoplasmic Reticulum Stress and Mitochondrial Dysfunction.International journal of molecular sciences · 2025Article
- Human antimicrobial/host defense peptide LL-37 may prevent the spread of a local infection through multiple mechanisms: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Article
- Insights into therapeutic peptides in the cancer-immunity cycle: Update and challenges.Acta pharmaceutica Sinica. B · 2024Review
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- Antimicrobial Peptides Mediate Apoptosis by Changing Mitochondrial Membrane Permeability.International journal of molecular sciences · 2022Review
- Renovation as innovation: Repurposing human antibacterial peptide LL-37 for cancer therapy.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human antimicrobial peptide LL-37 permeabilizes the plasma membrane of host cells, but LL-37-induced direct effects on mitochondrial membrane permeability and function has not been reported. Here, we demonstrate that LL-37 is rapidly (within 20 min) internalized by human osteoblast-like MG63 cells, and that the peptide co-localizes with MitoTracker arguing for accumulation in mitochondria. Subcellular fractionation and Western blot disclose that stimulation with LL-37 (8 μM) for 2 h triggers release of the mitochondrial protein apoptosis-inducing factor (AIF) to the cytosol, whereas LL-37 causes no release of cytochrome C oxidase subunit IV of the inner mitochondrial membrane, suggesting that LL-37 affects mitochondrial membrane permeability in a specific manner. Next, we investigated release of AIF and cytochrome C from isolated mitochondria by measuring immunoreactivity by dot blot. The media of mitochondria treated with LL-37 (8 μM) for 2 h contained 50% more AIF and three times more cytochrome C than that of control mitochondria, showing that LL-37 promotes release of both AIF and cytochrome C. Moreover, in vesicles reflecting mitochondrial membrane lipid composition, LL-37 stimulates membrane permeabilization and release of tracer molecules. We conclude that LL-37 is rapidly internalized by MG63 cells and accumulates in mitochondria, and that the peptide triggers release of pro-apoptotic AIF and directly affects mitochondrial membrane structural properties.
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