Oxidative Stress and Mitochondrial Dysfunction in Human Diseases: Pathophysiology, Predictive Biomarkers, Therapeutic

Li, Chia‐Jung

doi:10.3390/biom10111558

Cited by 5 publications

(4 citation statements)

References 6 publications

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“…There are a number of studies considering pro-inflammatory interleukins, oxidized lipoproteins, hypoxia, and oxidative stress from the perspective of cell apoptosis triggers in atherosclerotic plaques. 14,15 Bian W, in his study, showed that most of the apoptotic cells are localized in areas rich in activated T-lymphocytes and macrophages. In our study, in addition to an increase in the number of apoptosis markers, increases were also found in the values of PDGF BB and VEGF A165 markers.…”

Section: Discussionmentioning

confidence: 98%

Comprehensive assessment of markers of apoptosis and cell proliferation during progression of atherosclerosis after surgery in patients with peripheral arterial disease

2023

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Background Determination of predictors that can affect development of atherosclerosis progression in the postoperative period is an urgent problem in vascular surgery. Objectives Integrated assessment of markers of apoptosis and cell proliferation in atherosclerotic lesions and their progression after surgery in patients with peripheral arterial diseases. Methods The investigation included 30 patients with stage IIB-III peripheral arterial disease. All patients have undergone open surgical interventions on the arteries of the aorto-iliac and femoral-popliteal segments. During these interventions, intraoperative specimens were obtained from the vascular wall with atherosclerotic lesions. The following values were evaluated: VEGF А165, PDGF BB, and sFas. Samples of normal vascular wall were obtained from post-mortem donors and used as a control group. Results The levels of Bax and p53 were increased (p<0.001) in samples from arterial wall with atherosclerotic plaque, while sFas values were reduced (p<0.001), compared to their levels in control samples. Values of PDGF BB and VEGF A165 were 1.9 and 1.7 times higher in atherosclerotic lesion samples (p=0.001), in comparison with the control group. The levels of p53 and Bax were increased against a background of reduced sFas levels in samples with progression of atherosclerosis compared to their baseline values in samples with atherosclerotic plaque (p<0.05). Conclusions Initially increased values of the Bax marker against a background of reduced sFas values in vascular wall samples from patients with peripheral arterial disease is associated with risk of atherosclerosis progression in the postoperative period.

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Section: Discussionmentioning

confidence: 98%

Comprehensive assessment of markers of apoptosis and cell proliferation during progression of atherosclerosis after surgery in patients with peripheral arterial disease

2023

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“…The reactive oxygen species synthesized in mitochondria, also known as mtROS, is mainly generated due to proton leakage in the electron transport chain. In normal conditions, the production of one oxygen molecule requires the transfer of four electrons by the ETC after complex IV and four hydrogen ions are combined to form two H2O molecules ( Figure 1 ) [ 15 ].…”

Section: Three Ways That Mitochondrial Dysfunction Leads To Ramentioning

confidence: 99%

“…As mentioned above, ROS levels can increase dramatically due to certain environmental stresses (pathogenic factors) ( Figure 3 ). Excessive accumulation of ROS causes oxidative stress, which may lead to DNA damage, making mtDNA encode for the wrong polypeptide, which damages the mitochondria themselves and also leads to cellular dysfunction and disease [ 15 ]. ROS has an important role in the pathogenesis of RA.…”

Section: Etiology Of Mitochondrial Dysfunction In Ramentioning

confidence: 99%

Mitochondrial Dysfunction in Rheumatoid Arthritis

Wang

Hong

et al. 2022

Biomolecules

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Rheumatoid arthritis, a chronic autoimmune disease with complex etiology, is characterized by excessive proliferation of synovial cells, massive production of inflammatory cells and cartilage destruction. Studies have shown that mitochondrial dysfunction plays an important role in promoting the occurrence of RA. Mitochondria with normal structure and function are essential for the normal survival of chondrocytes and synovial cells. Once mitochondrial function is destroyed, it will affect the survival, activation and differentiation of immune cells and non-immune cells involved in the pathogenesis of RA, thus leading to the occurrence of RA. However, the mechanism of mitochondrial dysfunction in RA remains unclear. This article reviews the method of mitochondrial dysfunction leading to RA, the effects of mitochondrial dysfunction on immune cells, the etiology of mitochondrial dysfunction in RA, and the pathology of mitochondrial dysfunction in RA. We also outline some drugs that can exert therapeutic effects on RA which are associated with modulating mitochondrial activity. The understanding and summary of mitochondrial dysfunction in RA may provide new research directions for pathological intervention and prevention of RA.

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“…Atualmente, não existe um biomarcador único para disfunção mitocondrial, já que pode ser multifatorial para avaliar, podem-se incluir desde testes histoquímicos, imunohistoquímicos e bioquímicos combinados com as técnicas de genética molecular de rápido desenvolvimento (miopatias mitocondriais), ou biomarcadores ou metabolômicas, que podem ser utilizados para diagnóstico precoce de doenças neurodegenerativas, diabetes, doenças cardiovasculares, hepáticas e ou renais [20][21][22][23] .…”

Section: Disfunção Mitocondrialunclassified

Nutrição celular: um padrão de cuidado

Giorelli,

Machado,

Addor

et al. 2021

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Aging can be related to a cognitive decline, as well as, poor functionality, frailty and may increase the risk of developing diseases such as: cancer, diabetes, cardiovascular diseases, musculoskeletal and/or neurodegenerative disorders - which contribute to a worse quality of life and increased risk of death. Nine factors can contribute to cell aging, which can be summarized in the mnemonic DESGASTAR. Cellular senescence contributes to immunosenescence, which generates a low degree of inflammation, mitochondrial dysfunction that contributes to the generation of reactive oxygen specimens (ROS). The reduction in glutathione levels can contribute to aging, in addition to promoting inflammation and/or production of free radicals, which can contribute to an increased risk of chronic degenerative diseases. Interventions that include lifestyle changes (balanced diet, regular exercise, no smoking and moderate or non-consumption of alcohol), in addition to amino acid, vitamin and or mineral supplementation, when medically indicated and needed, can delay the physiological process called age-associated cell decline.

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Oxidative Stress and Mitochondrial Dysfunction in Human Diseases: Pathophysiology, Predictive Biomarkers, Therapeutic

Abstract: Mitochondria are important sites for a variety of cellular processes, including amino acid and fatty acid metabolism, the citric acid cycle, nitrogen metabolism, and oxidative phosphorylation to produce ATP [...]

Cited by 5 publications

References 6 publications

Comprehensive assessment of markers of apoptosis and cell proliferation during progression of atherosclerosis after surgery in patients with peripheral arterial disease

Comprehensive assessment of markers of apoptosis and cell proliferation during progression of atherosclerosis after surgery in patients with peripheral arterial disease

Mitochondrial Dysfunction in Rheumatoid Arthritis

Nutrição celular: um padrão de cuidado

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