Uncoupling protein 2 (UCP2) is an inner mitochondrial membrane protein that belongs to the uncoupling protein family and plays an important role in lowering mitochondrial membrane potential and dissipating metabolic energy with prevention of oxidative stress accumulation. In the present article, we will review the evidence that UCP2, as a consequence of its roles within the mitochondria, represents a critical player in the predisposition to vascular disease development in both animal models and in humans, particularly in relation to obesity, diabetes, and hypertension. The deletion of the UCP2 gene contributes to atherosclerosis lesion development in the knockout mice, also showing significantly shorter lifespan. The UCP2 gene downregulation is a key determinant of higher predisposition to renal and cerebrovascular damage in an animal model of spontaneous hypertension and stroke. In contrast, UCP2 overexpression improves both hyperglycemia- and high-salt diet-induced endothelial dysfunction and ameliorates hypertensive target organ damage in SHRSP. Moreover, drugs (fenofibrate and sitagliptin) and several vegetable compounds (extracts from Brassicaceae, berberine, curcumin, and capsaicin) are able to induce UCP2 expression level and to exert beneficial effects on the occurrence of vascular damage. As a consequence, UCP2 becomes an interesting therapeutic target for the treatment of common human vascular diseases.

Uncoupling protein 2: a key player and a potential therapeutic target in vascular diseases / Pierelli, Giorgia; Stanzione, Rosita; Forte, Maurizio; Migliarino, Serena; Perelli, Marika; Volpe, Massimo; Rubattu, Speranza. - In: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY. - ISSN 1942-0900. - ELETTRONICO. - 2017:(2017), pp. 7348372-7348383. [10.1155/2017/7348372]

Uncoupling protein 2: a key player and a potential therapeutic target in vascular diseases

Stanzione, Rosita
Methodology
;
Migliarino, Serena
Writing – Original Draft Preparation
;
Volpe, Massimo
Supervision
;
Rubattu, Speranza
Writing – Review & Editing
2017

Abstract

Uncoupling protein 2 (UCP2) is an inner mitochondrial membrane protein that belongs to the uncoupling protein family and plays an important role in lowering mitochondrial membrane potential and dissipating metabolic energy with prevention of oxidative stress accumulation. In the present article, we will review the evidence that UCP2, as a consequence of its roles within the mitochondria, represents a critical player in the predisposition to vascular disease development in both animal models and in humans, particularly in relation to obesity, diabetes, and hypertension. The deletion of the UCP2 gene contributes to atherosclerosis lesion development in the knockout mice, also showing significantly shorter lifespan. The UCP2 gene downregulation is a key determinant of higher predisposition to renal and cerebrovascular damage in an animal model of spontaneous hypertension and stroke. In contrast, UCP2 overexpression improves both hyperglycemia- and high-salt diet-induced endothelial dysfunction and ameliorates hypertensive target organ damage in SHRSP. Moreover, drugs (fenofibrate and sitagliptin) and several vegetable compounds (extracts from Brassicaceae, berberine, curcumin, and capsaicin) are able to induce UCP2 expression level and to exert beneficial effects on the occurrence of vascular damage. As a consequence, UCP2 becomes an interesting therapeutic target for the treatment of common human vascular diseases.
2017
proliferator-activated receptor; spontaneously hypertensive-rats; necrosis-factor-alpha; oxidative stress; diabetic-retinopathy; gene-expression; renal damage; organ damage; UCP2 gene; AMPK/PPAR-ALPHA/UCP2 AXIS
01 Pubblicazione su rivista::01a Articolo in rivista
Uncoupling protein 2: a key player and a potential therapeutic target in vascular diseases / Pierelli, Giorgia; Stanzione, Rosita; Forte, Maurizio; Migliarino, Serena; Perelli, Marika; Volpe, Massimo; Rubattu, Speranza. - In: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY. - ISSN 1942-0900. - ELETTRONICO. - 2017:(2017), pp. 7348372-7348383. [10.1155/2017/7348372]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1072946
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