The Pivotal Role of Oxidative Stress in the Pathophysiology of Cardiovascular-Renal Remodeling in Kidney Disease

Ravarotto, Verdiana; Bertoldi, Giovanni; Innico, Georgie; Gobbi, Laura; Calò, Lorenzo A.

doi:10.3390/antiox10071041

Cited by 18 publications

(12 citation statements)

References 93 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NOX2-mediated ROS play an important pathogenetic role in different kidney diseases. Angiotensin-converting enzyme-2 attenuates diabetic kidney injury in the Akita mouse model in association with decreased NOX2 activity ( 20 ). It has been shown that NOX2 modulates ischemia–reperfusion injury in delayed graft function and that its absence is associated with reduced inflammation and fibrosis ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

et al. 2023

View full text Add to dashboard Cite

BackgroundsCisplatin is a commonly used chemotherapeutic agent in cancer treatment. However, its high nephrotoxicity limits its therapeutic application and efficacy. Cisplatin induces nephrotoxicity mainly through oxidative stress and inflammation. Reactive oxygen species (ROS) in the kidneys mainly arise from nicotinamide adenine dinucleotide phosphate (NADPH) oxidases 2 (NOX2), which is highly upregulated during ischemia-reperfusion injury and diabetes mellitus. However, its role in cisplatin-induced acute kidney injury (AKI) remains unknown.MethodsA 8-10-week-old NOX2 gene-knockout and wild-type mice were injected with 25 mg/kg cisplatin intraperitoneally for experiments.ResultsWe investigated the role of NOX2 in cisplatin-induced AKI and found that NOX2-mediated ROS production is a key inflammatory mediator of proximal tubular cell injury in cisplatin-induced AKI. NOX2 gene-knockout alleviated cisplatin-induced renal function decline, tubular injury score, kidney injury molecule-1(Kim-1) expression, and interleukin (IL)-6 and IL-1α levels with a reduction of ROS production. Moreover, in cisplatin-induced AKI, intercellular adhesion molecule 1 (ICAM-1) and the chemoattractant CXC ligand 1 (CXCL1) were highly expressed in association with neutrophil infiltration, which were all attenuated by deletion of NOX2.ConclusionThese data indicate that NOX2 aggravates cisplatin nephrotoxicity by promoting ROS-mediated tissue injury and neutrophil infiltration. Thus, appropriate targeting of NOX2/ROS pathway may minimize the risk of cisplatin-induced kidney injury in patients receiving cancer therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

“…There are seven isoforms of the NOX family (NOX1–5, Duox1/2). Different NOX isoforms are regionally distributed along the nephron segments ( 19 , 20 ). The classic NOX2 is found primarily in phagocytic cells but is also expressed in renal proximal tubular cells.…”

Section: Introductionmentioning

confidence: 99%

Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Hence, utilizing RAS inhibition in prematurity-related kidney disease before 2 years of life is limited. Nonetheless, RAS activation is known to drive oxidative stress and fibrosis in kidney disease ( 146 ).…”

Section: Other Oxidative Stress Lowering Therapies To Avert Chronic K...mentioning

confidence: 99%

Educational Review: The Impact of Perinatal Oxidative Stress on the Developing Kidney

et al. 2022

View full text Add to dashboard Cite

Oxidative stress occurs when there is an imbalance between reactive oxygen species/reactive nitrogen species and antioxidant systems. The interplay between these complex processes is crucial for normal pregnancy and fetal development; however, when oxidative stress predominates, pregnancy related complications and adverse fetal programming such as preterm birth ensues. Understanding how oxidative stress negatively impacts outcomes for the maternal-fetal dyad has allowed for the exploration of antioxidant therapies to prevent and/or mitigate disease progression. In the developing kidney, the negative impact of oxidative stress has also been noted as it relates to the development of hypertension and kidney injury mostly in animal models. Clinical research addressing the implications of oxidative stress in the developing kidney is less developed than that of the neurodevelopmental and respiratory conditions of preterm infants and other vulnerable neonatal groups. Efforts to study the oxidative stress pathway along the continuum of the perinatal period using a team science approach can help to understand the multi-organ dysfunction that the maternal-fetal dyad sustains and guide the investigation of antioxidant therapies to ameliorate the global toxicity. This educational review will provide a comprehensive and multidisciplinary perspective on the impact of oxidative stress during the perinatal period in the development of maternal and fetal/neonatal complications, and implications on developmental programming of accelerated aging and cardiovascular and renal disease for a lifetime.

show abstract

“…On the other hand, hypertension is a common pathological event in CVD and CKD patients. Renal mitochondrial oxidative stress has been associated with renin-angiotensin system activation [18], leading to increased Angiotensin II and the subsequent induction of oxidative stress and, therefore, mitochondrial dysfunction in cardiovascular tissues, participating in the progression of damage [19]. These common pathological events demonstrate the close relationship between CKD-CVD and the important role of mitochondria in the context of CRS.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Dysfunction in the Cardio-Renal Axis

Oller

Sanz

Ramos

et al. 2023

IJMS

View full text Add to dashboard Cite

Cardiovascular disease (CVD) frequently complicates chronic kidney disease (CKD). The risk of all-cause mortality increases from 20% to 500% in patients who suffer both conditions; this is referred to as the so-called cardio-renal syndrome (CRS). Preclinical studies have described the key role of mitochondrial dysfunction in cardiovascular and renal diseases, suggesting that maintaining mitochondrial homeostasis is a promising therapeutic strategy for CRS. In this review, we explore the malfunction of mitochondrial homeostasis (mitochondrial biogenesis, dynamics, oxidative stress, and mitophagy) and how it contributes to the development and progression of the main vascular pathologies that could be affected by kidney injury and vice versa, and how this knowledge may guide the development of novel therapeutic strategies in CRS.

show abstract

The Pivotal Role of Oxidative Stress in the Pathophysiology of Cardiovascular-Renal Remodeling in Kidney Disease

Cited by 18 publications

References 93 publications

Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

Deletion of NADPH oxidase 2 attenuates cisplatin-induced acute kidney injury through reducing ROS-induced proximal tubular cell injury and inflammation

Educational Review: The Impact of Perinatal Oxidative Stress on the Developing Kidney

Mitochondrial Dysfunction in the Cardio-Renal Axis

Contact Info

Product

Resources

About