Mitochondria-targeted cytoprotective peptides for ischemia-reperfusion injury.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing in vitro, cellular, and animal research
PubMed 17999629 · doi:10.1089/ars.2007.1892
What was done
This review summarized preclinical literature on cell-permeable Szeto-Schiller (SS) peptides, examining their localization, biochemical actions in isolated mitochondria and cell cultures, and therapeutic efficacy across animal models of ischemia-reperfusion injury, neurodegeneration, and renal fibrosis.
What was found
The abstract provides qualitative descriptions without numerical data. SS peptides selectively partition to the inner mitochondrial membrane, scavenge reactive oxygen species (ROS), decrease mitochondrial ROS generation, and inhibit mitochondrial permeability transition. They prevent oxidative stress- and electron transport chain inhibition-induced apoptosis and necrosis, demonstrating cytoprotective efficacy and an absence of apparent toxicity in animal disease models.
Why it matters
Highlights the mechanistic rationale and early preclinical proof-of-concept for peptide-based delivery of antioxidant and cytoprotective agents directly to the inner mitochondrial membrane.
Limits
The abstract describes a narrative review restricted to in vitro and animal models with no human clinical evaluation. Quantitative effect sizes, comparative efficacy across specific peptide variants, and study sample sizes are not reported.
Cited by
- supports The peptide SS-31 was discovered by Hazel Szeto.