The role of oxidative stress-mediated apoptosis in the pathogenesis of uric acid nephropathy

Yang, Lijuan; Chang, Baochao; Guo, Yaling; Wu, Xin; Liu, Lei

doi:10.1080/0886022x.2019.1633350

Cited by 50 publications

(41 citation statements)

References 17 publications

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“…For example, the vehicle utilized to formulate the PAHSA is critical not only to assure bioavailability and safety but also to avoid masking the effects of PAHSA. In NASH, in addition to metabolic disturbance, the accumulation of lipids in hepatocytes, oxidative stress and decreased ATP production trigger mitochondrial dysfunction [18]. In the current work, we showed an additional protective function of 9-PAHSA in an in vitro model of steatosis.…”

Section: Discussionsupporting

confidence: 60%

9-PAHSA Prevents Mitochondrial Dysfunction and Increases the Viability of Steatotic Hepatocytes

Moreira

Rüschenbaum

Schefczyk

et al. 2020

IJMS

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Nonalcoholic fatty liver disease (NAFLD) is quickly becoming the most common liver disease worldwide. Within the NAFLD spectrum, patients with nonalcoholic steatohepatitis (NASH) are at the highest risk of developing cirrhosis and disease progression to hepatocellular carcinoma. To date, therapeutic options for NASH patients have been ineffective, and therefore, new options are urgently needed. Hence, a model system to develop new therapeutic interventions is needed. Here, we introduce two new in vitro models of steatosis induction in HepG2 cells and primary murine hepatocytes. We used a recently discovered novel class of bioactive anti-inflammatory lipids called branched fatty acid esters of hydroxyl fatty acids. Among these bioactive lipids, palmitic-acid-9-hydroxy-stearic-acid (9-PAHSA) is the most promising as a representative nondrug therapy based on dietary supplements or nutritional modifications. In this study, we show a therapeutic effect of 9-PAHSA on lipotoxicity in steatotic primary hepatocytes and HepG2 cells. This could be shown be increased viability and decreased steatosis. Furthermore, we could demonstrate a preventive effect in HepG2 cells. The outcome of 9-PAHSA administration is both preventative and therapeutically effective for hepatocytes with limited damage. In conclusion, bioactive lipids like 9-PAHSA offer new hope for prevention or treatment in patients with fatty liver and steatosis.

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Section: Discussionsupporting

confidence: 60%

9-PAHSA Prevents Mitochondrial Dysfunction and Increases the Viability of Steatotic Hepatocytes

Moreira

Rüschenbaum

Schefczyk

et al. 2020

IJMS

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“…Many studies have shown that hyperuricemia-induced oxidative stress affects multiple organs and systems, including the kidneys [ 42 – 44 ]. Pathologically, hyperuricemia-associated oxidative stress gives rise to DNA damage, oxidation and inactivation of enzymes, inflammatory cytokine production, and cell apoptosis [ 45 ].…”

Section: Mechanisms Of Hyperuricemia-induced Renal Injurymentioning

confidence: 99%

“…Meanwhile, it has been reported that hyperuricemia induced endothelial dysfunction via regulation of AR, while inhibition of AR or degradation of ROS could restore endothelial function [ 51 ]. Similarly, antioxidant therapies, such as tempol and reduced GSH, may be beneficial for the recovery of endothelial function [ 45 , 46 ]. Taken together, hyperuricemia-mediated oxidative stress directly damages the kidney, thus being a biotherapeutic target for UA-induced renal damage.…”

Section: Mechanisms Of Hyperuricemia-induced Renal Injurymentioning

confidence: 99%

Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury

Yang

Liang

et al. 2020

BioMed Research International

117

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Uric acid is the end product of purine metabolism in humans, and its excessive accumulation leads to hyperuricemia and urate crystal deposition in tissues including joints and kidneys. Hyperuricemia is considered an independent risk factor for cardiovascular and renal diseases. Although the symptoms of hyperuricemia-induced renal injury have long been known, the pathophysiological molecular mechanisms are not completely understood. In this review, we focus on the research advances in the mechanisms of hyperuricemia-caused renal injury, primarily on oxidative stress, endothelial dysfunction, renal fibrosis, and inflammation. Furthermore, we discuss the progress in hyperuricemia management.

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“…The increase in uric acid synthesis damages renal functions, which can be explained by direct promotion of oxidative stress. Increased uric acid synthesis can promote oxidative stress by generating superoxide radicals which can stimulate the mitochondrial membrane lipid peroxidation, mitochondrial dysfunction and cell apoptosis (22).…”

Section: Egfr and Serum Creatininementioning

confidence: 99%

“…The mitochondrial membrane lipid peroxidation occurs when uncontrolled free oxygen radicals are produced. Lipid peroxidation participates in reducing the membrane fl uidity that can lead to mitochondrial swelling, mitochondrial dysfunction, and apoptosis of renal tubule epithelial cells (22). The major sites of mitochondrial ROS generation are at complex I and complex III.…”

Section: Plasma Coq 10-total In Subgroups Of Ckd Patients With Concommentioning

confidence: 99%

The importance of coenzyme Q10 and its ratio to cholesterol in the progress of chronic kidney diseases linked to non- -communicable diseases

Gvozdjáková¹,

Kucharská²,

Sumbalová³

et al. 2020

BLL

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OBJECTIVES: The mortality of patients with chronic kidney diseases (CKD) increases with the decrease in glomerular fi ltration rate (eGFR). In the progress of CKD that is closely linked to non-communicable diseases (NCDs), the role of coenzyme Q 10 (CoQ 10) is not fully evaluated. We aimed to evaluate the importance of CoQ 10, CoQ 10 /cholesterol ratio, and oxidative stress in the progress of CKD. PATIENTS AND METHODS: The control group was constituted of 19 healthy subjects who volunteered to enrol in the study, CKD group consisted of 58 patients with CKD, of whom 54 had CKD combined with hypertension, 22 had CKD combined with hypertension and diabetes type 2 , and 18 had CKD combined with hypertension and statin therapy. We observed age, BMI, creatinine, uric acid, eGFR, hemoglobin, CRP, glucose, lipids fraction, and liver enzymes. Coenzyme Q 10-TOTAL (ubiquinol+ubiquinone) in platelets and plasma were determined using HPLC method with UV detection. Indexed of CoQ 10 /lipid fractions were evaluated. Oxidative stress was determined as thiobarbituric acid-reactive substances (TBARS). RESULTS: With increased stages of CKD, eGFR and CoQ 10 as well as its ratio to lipids were signifi cantly reduced while TBARS increased. CONCLUSION: We assume that lower endogenous CoQ 10 level may be one of the reasons of kidney dysfunction. CoQ 10 /lipids ratio and increase in oxidative stress can predict the progression of CKD in patients with arterial hypertension, diabetes mellitus and dyslipidemia (Tab. 2, Fig. 4, Ref. 49). Text in PDF www.elis.sk KEY WORDS: chronic kidney disease, non-communicable diseases, glomerular fi ltration, creatinine, coenzyme Q 10, oxidative stress, index of CoQ 10-TOTAL /lipids.

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The role of oxidative stress-mediated apoptosis in the pathogenesis of uric acid nephropathy

Cited by 50 publications

References 17 publications

9-PAHSA Prevents Mitochondrial Dysfunction and Increases the Viability of Steatotic Hepatocytes

9-PAHSA Prevents Mitochondrial Dysfunction and Increases the Viability of Steatotic Hepatocytes

Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury

The importance of coenzyme Q10 and its ratio to cholesterol in the progress of chronic kidney diseases linked to non- -communicable diseases

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