The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes.

Escribano-Lopez I, Diaz-Morales N, Iannantuoni F, Lopez-Domenech S, de Marañon AM, Abad-Jimenez Z, Bañuls C, Rovira-Llopis S, Herance JR, Rocha M, Victor VM

Scientific reports26 Oct 2018Cited by 58 (Europe PMC)

PMID30367115PMCIDPMC6203778DOI10.1038/s41598-018-34251-8PepBankPUB-30367115

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Summary

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.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

9 results from studies that gave the peptide. No result from this study comes from people.

01LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 treatment restored the increased mitochondrial ROS production.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 lowered raised mitochondrial ROS.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseMitochondrial ROS production
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Oxidative stress · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
We observed increased mitochondrial ROS production that was restored by SS-31 treatment.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711501
02LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 increased mitochondrial membrane potential.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 raised mitochondrial membrane potential.
Peptide
Elamipretide (SS-31)
Outcome
IncreaseMitochondrial membrane potential
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Mitochondrial function · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velocity and reduced rolling flux and adhesion in T2D patients.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711502
03LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 increased glutathione content.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 raised glutathione content.
Peptide
Elamipretide (SS-31)
Outcome
IncreaseGlutathione content
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Oxidative stress · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velocity and reduced rolling flux and adhesion in T2D patients.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711503
04LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 increased SIRT1 levels.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 raised SIRT1 levels.
Peptide
Elamipretide (SS-31)
Outcome
IncreaseSIRT1 level
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Aging markers · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velocity and reduced rolling flux and adhesion in T2D patients.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711504
05LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 increased leukocyte rolling velocity.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 sped up cell rolling along vessel walls.
Peptide
Elamipretide (SS-31)
Outcome
IncreaseLeukocyte rolling velocity
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Vascular function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velocity and reduced rolling flux and adhesion in T2D patients.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711505
06LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 reduced leukocyte rolling flux.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 lowered the number of cells rolling along vessel walls.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseLeukocyte rolling flux
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Vascular function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velocity and reduced rolling flux and adhesion in T2D patients.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711506
07LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 reduced leukocyte adhesion.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 reduced sticking of cells to vessel walls.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseLeukocyte adhesion
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Vascular function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
SS-31 also increased mitochondrial membrane potential, glutathione content, SIRT1 levels and leukocyte rolling velocity and reduced rolling flux and adhesion in T2D patients.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711507
08LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 treatment reduced the enhanced NFκB-p65 level.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 lowered raised NFκB-p65 levels.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseNFκB-p65 level
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
NFκB-p65 and TNFα, which were enhanced in diabetic patients, were also reduced by SS-31 treatment.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711508
09LabEx vivo tissueMechanism
In leukocytes from patients with type 2 diabetes, SS‑31 treatment reduced the enhanced TNFα level.
In plain wordsIn lab tests on white blood cells with type 2 diabetes origin, SS‑31 lowered raised TNFα levels.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseTNFα level
Study
humann: not reported in source
leukocytes from patients with type 2 diabetes
Comparator
Untreated leukocytes
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
NFκB-p65 and TNFα, which were enhanced in diabetic patients, were also reduced by SS-31 treatment.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-3036711509

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 08:19 UTC
Study results updated
Version 1
9 Oct 2026, 02:47 UTC
First added · source update from Europe PMC

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