ArticleScientific reports2018
The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 69 citations in OpenAlex.
- Mitochondria as a Therapeutic Target in Metabolic Disorders.Mini reviews in medicinal chemistry · 2026Review
- Mitochondrial dysfunction, reactive oxygen species, and diabetes mellitus - A triangular relationship: A review.Biomolecules & biomedicine · 2025Review
- Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction.International journal of molecular sciences · 2025Review
- The mitochondrial protectant SS31 optimized decellularized Wharton's jelly scaffold improves allogeneic chondrocyte implantation-mediated articular cartilage repair.Journal of orthopaedic translation · 2025Article
- Protective Role and Enhanced Intracellular Uptake of Curcumin in Retinal Cells Using Self-Emulsifying Drug Delivery Systems (SNEDDS).Pharmaceuticals (Basel, Switzerland) · 2025Article
- Podocyte senescence: from molecular mechanisms to therapeutics.Renal failure · 2024Review
- Autophagy and mitophagy as potential therapeutic targets in diabetic heart condition: Harnessing the power of nanotheranostics.Asian journal of pharmaceutical sciences · 2024Review
- Mitochondrial antioxidant elamipretide improves learning and memory impairment induced by chronic sleep deprivation in mice.Brain and behavior · 2024Article
- Mechanisms of Modulation of Mitochondrial Architecture.Biomolecules · 2023Review
- Exploring the Complex Relationship between Diabetes and Cardiovascular Complications: Understanding Diabetic Cardiomyopathy and Promising Therapies.Biomedicines · 2023Review
- A new triphenylphosphonium-conjugated amphipathic cationic peptide with improved cell-penetrating and ROS-targeting properties.Current research in pharmacology and drug discovery · 2023Article
- Bone-Muscle Crosstalk: Musculoskeletal Complications of Chemotherapy.Current osteoporosis reports · 2022Review
- Targeting mitochondrial bioenergetics as a promising therapeutic strategy in metabolic and neurodegenerative diseases.Biomedical journal · 2022Review
- Mitochondrial and metabolic dysfunction in ageing and age-related diseases.Nature reviews. Endocrinology · 2022Review
- SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022Review
- Review
- Mitochondria in Diabetic Kidney Disease.Cells · 2021Review
- SIRT1 Mediates HNeurochemical research · 2021Article
- Targeting Mitochondria by SS-31 Ameliorates the Whole Body Energy Status in Cancer- and Chemotherapy-Induced Cachexia.Cancers · 2021Article
- Mitochondrial-Targeting Antioxidant SS-31 Suppresses Airway Inflammation and Oxidative Stress Induced by Cigarette Smoke.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
There is growing focus on mitochondrial impairment and cardiovascular diseases (CVD) in type 2 diabetes (T2D), and the development of novel therapeutic strategies in this context. It is unknown whether mitochondrial-targeting antioxidants such as SS-31 protect sufficiently against oxidative damage in diabetes. We aimed to evaluate if SS-31 modulates SIRT1 levels and ameliorates leukocyte-endothelium interactions, oxidative stress and inflammation in T2D patients. Anthropometric and metabolic parameters were studied in 51 T2D patients and 57 controls. Production of mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential, glutathione content, leukocyte-endothelium interactions, NFκB-p65, TNFα and SIRT1 levels was measured in leukocytes treated or not with SS-31. We observed increased mitochondrial ROS production that was restored by SS-31 treatment. SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velocity and reduced rolling flux and adhesion in T2D patients. NFκB-p65 and TNFα, which were enhanced in diabetic patients, were also reduced by SS-31 treatment. Our results reveal that SS-31 exerts beneficial effects on the leukocytes of T2D patients by reducing oxidative stress, leukocyte-endothelium interactions, NFκB and TNFα and by increasing SIRT1 levels. These actions support its use as a potential agent against CVD risk.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.