Diabetes-related vascular complication rates remain unacceptably high despite guideline-based
medical therapies that are significantly more effective in individuals without diabetes.
This critical gap represents an opportunity for researchers and clinicians to collaborate
on targeting mechanisms and pathways that specifically contribute to vascular pathology
in patients with diabetes mellitus. Dysfunctional mitochondria producing excessive
mitochondrial reactive oxygen species (mtROS) play a proximal cell-signaling role
in the development of vascular endothelial dysfunction in the setting of diabetes.
Targeting the mechanisms of production of mtROS or mtROS themselves represents an
attractive method to reduce the prevalence and severity of diabetic vascular disease.
This review focuses on the role of mitochondria in the development of diabetic vascular
disease and current developments in methods to improve mitochondrial health to improve
vascular outcomes in patients with DM.
- Abbreviations: CuZn SOD
- copper-zinc superoxide dismutase
- DM
- diabetes mellitus
- Drp1
- dynamin-related protein 1
- ETC
- electron transport chain
- FFA
- free fatty acids
- HUVECs
- human umbilical vein endothelial cells
- MnSOD
- manganese superoxide dismutase
- Mdivi-1
- mitochondrial division inhibitor 1
- Δψm
- mitochondrial membrane potential
- Mfn1/2
- mitofusin 1/2
- mPTP
- mitochondrial permeability transition pore
- mtROS
- mitochondrial reactive oxygen species
- NMN
- nicotinamide mononucleotide
- NR
- nicotinamide riboside
- NO
- nitric oxide
- OPA-1
- optic atrophy protein 1
- SIRT1
- sirtuin-1
- SS
- Szeto-Schiller
- UCP2
- uncoupling protein 2
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Article info
Publication history
Published online: August 03, 2018
Accepted:
July 27,
2018
Received in revised form:
July 9,
2018
Received:
April 22,
2018
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© 2018 Elsevier Inc. All rights reserved.