ArticleMolecules (Basel, Switzerland)2015
Mitochondrion-Targeted Peptide SS-31 Inhibited Oxidized Low-Density Lipoproteins-Induced Foam Cell Formation through both ROS Scavenging and Inhibition of Cholesterol Influx in RAW264.7 Cells.
Article in Molecules (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026Review
- Mitochondria as a Therapeutic Target in Metabolic Disorders.Mini reviews in medicinal chemistry · 2026Review
- Histone demethylase JMJD1C advances macrophage foam cell formation and atherosclerosis progression by promoting the transcription of PCSK9.Journal of physiology and biochemistry · 2025Article
- Advances in the treatment of lower-extremity ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Engineering Macrophage via Biomaterial-Mediated Mitochondrial Regulation: Mechanisms and Strategies.Research (Washington, D.C.) · 2025Review
- Mitochondrial antioxidant elamipretide improves learning and memory impairment induced by chronic sleep deprivation in mice.Brain and behavior · 2024Article
- Targeted Treatment Strategies for Mitochondria Dysfunction: Correlation with Neurological Disorders.Current drug targets · 2024Review
- Advancements in mitochondrial-targeted nanotherapeutics: overcoming biological obstacles and optimizing drug delivery.Frontiers in immunology · 2024Review
- Activation of NLRP3 Inflammasome via Drp1 Overexpression in Kupffer Cells Aggravates Ischemia-reperfusion Injury in Hepatic Steatosis.Journal of clinical and translational hepatology · 2023Article
- Antibiotic pretreatment attenuates liver ischemia-reperfusion injury by Farnesoid X receptor activation.Cell death & disease · 2022Article
- The elevation of miR-185-5p alleviates high-fat diet-induced atherosclerosis and lipid accumulationAging · 2022Article
- Isoflavones from Semen Sojae Preparatum Improve Atherosclerosis and Oxidative Stress by Modulating Nrf2 Signaling Pathway through Estrogen-Like Effects.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022Review
- Mitochondria-targeted nanoparticles in treatment of neurodegenerative diseases.Exploration (Beijing, China) · 2021Review
- SS-31 Protects Liver from Ischemia-Reperfusion Injury via Modulating Macrophage Polarization.Oxidative medicine and cellular longevity · 2021Article
- Iron accumulation in macrophages promotes the formation of foam cells and development of atherosclerosis.Cell & bioscience · 2020Article
- Neutralizing mitochondrial ROS does not rescue muscle atrophy induced by hindlimb unloading in female mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- SS-31 Peptide Reverses the Mitochondrial Fragmentation Present in Fibroblasts From Patients With DCMA, a Mitochondrial Cardiomyopathy.Frontiers in cardiovascular medicine · 2019Article
- The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes.Scientific reports · 2018Article
- Protective effects of mitochondrion-targeted peptide SS-31 against hind limb ischemia-reperfusion injury.Journal of physiology and biochemistry · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foam cell formation as a result of imbalance of modified cholesterol influx and efflux by macrophages is a key to the occurrence and development of atherosclerosis. Oxidative stress is thought to be involved in the pathogenesis of atherosclerosis. SS-31 is a member of the Szeto-Schiller (SS) peptides shown to specifically target the inner mitochondrial membrane to scavenge reactive oxygen species. In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells. The results showed that SS-31 inhibited oxidized low-density lipoproteins (ox-LDL)-induced foam cell formation and cholesterol accumulation, demonstrated by intracellular oil red O staining and measurement of cholesterol content. The mechanism was revealed that SS-31 did not only significantly attenuated ox-LDL-induced generation of reactive oxygen species (ROS) and increased the activities of superoxide dismutases, but also dose-dependently inhibited the expression of CD36 and LOX-1, two scavenger receptors of ox-LDL, while the expression of ATP-binding cassette A1 and G1, playing a pivotal role in cholesterol efflux, was not affected. As a result, SS-31 decreased pro-inflammatory cytokines such as interleukin 6 and tumor necrosis factor alpha, suggesting the prevention of inflammatory responses. In conclusion, our results demonstrate that SS-31 provides a beneficial effect on macrophages from foam cell formation, likely, through both ROS scavenging and inhibition of cholesterol influx. Therefore, SS-31 may potentially be of therapeutic relevance in prevention of human atherogenesis.
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