Peripheral Arterial Disease and Oxidative Stress

2007 ◽  
Vol 4 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Francesco Violi ◽  
Lorenzo Loffredo
2006 ◽  
Vol 44 (3) ◽  
pp. 525-530 ◽  
Author(s):  
Lorenzo Loffredo ◽  
Pasquale Pignatelli ◽  
Roberto Cangemi ◽  
Paola Andreozzi ◽  
Maria Antonietta Panico ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2220-PUB
Author(s):  
MATHILDE NATIVEL ◽  
FABRICE SCHNEIDER ◽  
PIERRE SAULNIER ◽  
OLIVIER MEILHAC ◽  
PHILIPPE RONDEAU ◽  
...  

2020 ◽  
Vol 11 ◽  
pp. 204062231989446
Author(s):  
Salvatore Santo Signorelli ◽  
Luca Vanella ◽  
Nader G. Abraham ◽  
Salvatore Scuto ◽  
Elisa Marino ◽  
...  

Peripheral arterial disease (PAD) affects individuals particularly over 65 years old in the more advanced countries. Hemodynamic, inflammatory, and oxidative mechanisms interact in the pathophysiological scenario of this chronic arterial disease. We discuss the hemodynamic, muscle tissue, and oxidative stress (OxS) conditions related to chronic ischemia of the peripheral arteries. This review summarizes the results of evaluating both metabolic and oxidative markers, and also therapy to counteract OxS. In conclusion, we believe different pathways should be highlighted to discover new drugs to treat patients suffering from PAD.


2006 ◽  
Vol 28 (5) ◽  
pp. 608-612 ◽  
Author(s):  
L. Loffredo ◽  
A. Marcoccia ◽  
P. Pignatelli ◽  
P. Andreozzi ◽  
M.C. Borgia ◽  
...  

Vascular ◽  
2020 ◽  
pp. 170853812094724
Author(s):  
Ufuk Turan Kursat Korkmaz ◽  
Ahmet Yuksel ◽  
Ayhan Cetinkaya ◽  
Yusuf Velioglu ◽  
Erhan Renan Ucaroglu ◽  
...  

Objective To examine dynamic thiol/disulphide homeostasis metrics as a novel risk factor of oxidative stress in patients with peripheral arterial disease. Methods One hundred patients with lower extremity peripheral arterial disease (a study group) and 100 control subjects were included in this prospective case–control study. Participants’ baseline clinical characteristics and laboratory data including some oxidant/antioxidant status parameters such as albumin, ferroxidase and myeloperoxidase, and thiol/disulphide homeostasis parameters such as native thiol, total thiol and disulphide, as well as native thiol/total thiol, disulphide/native thiol and disulphide/total thiol ratios were all recorded and then compared between the groups. Results Mean albumin and ferroxidase, and median myeloperoxidase levels were found to be significantly higher in patients with the peripheral arterial disease than in control group ( p = 0.045, p = 0.000 and p = 0.000, respectively). Mean native thiol and total thiol, and median disulphide levels were found to be significantly lower in the study group as compared with the control group ( p = 0.000, p = 0.000 and p = 0.037, respectively). According to the results of logistic regression analysis, systolic blood pressure, ferroxidase and myeloperoxidase levels were detected to be the independent predictors of peripheral arterial disease. Conclusion Our report is the first one in the literature investigating dynamic thiol/disulphide homeostasis metrics as a novel risk factor of oxidative stress in peripheral arterial disease. Dynamic thiol/disulphide homeostasis metrics may be used as a valuable risk factor of oxidative stress in patients with the peripheral arterial disease since it is readily available, easily calculated and relatively cheap.


2007 ◽  
Vol 8 (1) ◽  
pp. 115
Author(s):  
L. Loffredo ◽  
A. Marcoccia ◽  
P. Pignatelli ◽  
P. Andreozzi ◽  
L. Perri ◽  
...  

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1304
Author(s):  
Kyoungrae Kim ◽  
Erik M. Anderson ◽  
Salvatore T. Scali ◽  
Terence E. Ryan

Peripheral artery disease (PAD) is caused by atherosclerosis in the lower extremities, which leads to a spectrum of life-altering symptomatology, including claudication, ischemic rest pain, and gangrene requiring limb amputation. Current treatments for PAD are focused primarily on re-establishing blood flow to the ischemic tissue, implying that blood flow is the decisive factor that determines whether or not the tissue survives. Unfortunately, failure rates of endovascular and revascularization procedures remain unacceptably high and numerous cell- and gene-based vascular therapies have failed to demonstrate efficacy in clinical trials. The low success of vascular-focused therapies implies that non-vascular tissues, such as skeletal muscle and oxidative stress, may substantially contribute to PAD pathobiology. Clues toward the importance of skeletal muscle in PAD pathobiology stem from clinical observations that muscle function is a strong predictor of mortality. Mitochondrial impairments in muscle have been documented in PAD patients, although its potential role in clinical pathology is incompletely understood. In this review, we discuss the underlying mechanisms causing mitochondrial dysfunction in ischemic skeletal muscle, including causal evidence in rodent studies, and highlight emerging mitochondrial-targeted therapies that have potential to improve PAD outcomes. Particularly, we will analyze literature data on reactive oxygen species production and potential counteracting endogenous and exogenous antioxidants.


2011 ◽  
Vol 11 (6) ◽  
pp. 453-464 ◽  
Author(s):  
A. Rull ◽  
R. Garcia ◽  
L. Fernandez-Sender ◽  
R. Beltran-Debon ◽  
G. Aragones ◽  
...  

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