Oxidative stress as a potential target in acute kidney injury

Abstract

BackgroundAcute kidney injury (AKI) is a major problem for health systems being directly related to short and long-term morbidity and mortality. In the last years, the incidence of AKI has been increasing. AKI and chronic kidney disease (CKD) are closely interconnected, with a growing rate of CKD linked to repeated and severe episodes of AKI. AKI and CKD can occur also secondary to imbalanced oxidative stress (OS) reactions, inflammation, and apoptosis. The kidney is particularly sensitive to OS. OS is known as a crucial pathogenetic factor in cellular damage, with a direct role in initiation, development, and progression of AKI. The aim of this review is to focus on the pathogenetic role of OS in AKI in order to gain a better understanding. We exposed the potential relationships between OS and the perturbation of renal function and we also presented the redox-dependent factors that can contribute to early kidney injury. In the last decades, promising advances have been made in understanding the pathophysiology of AKI and its consequences, but more studies are needed in order to develop new therapies that can address OS and oxidative damage in early stages of AKI.MethodsWe searched PubMed for relevant articles published up to May 2019. In this review we incorporated data from different types of studies, including observational and experimental, both in vivo and in vitro, studies that provided information about OS in the pathophysiology of AKI.ResultsThe results show that OS plays a major key role in the initiation and development of AKI, providing the chance to find new targets that can be therapeutically addressed.DiscussionAcute kidney injury represents a major health issue that is still not fully understood. Research in this area still provides new useful data that can help obtain a better management of the patient. OS represents a major focus point in many studies, and a better understanding of its implications in AKI might offer the chance to fight new therapeutic strategies.

Echinacea polysaccharide attenuates lipopolysaccharide‑induced acute kidney injury via inhibiting inflammation, oxidative stress and the MAPK signaling pathway

“…OS serves an important role in the occurrence and development of AKI ( 44 ). It has been demonstrated that OS is enhanced in LPS-induced models of AKI ( 45 ) and that the MAPK signaling pathway is an essential modulator of altered gene transcription in response to increased OS ( 46 ).…”

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“…Both acute kidney injury (AKI) and chronic kidney disease (CKD) have been associated with decreased antioxidant defense and/or increased ROS that contribute to the disease progression [ 3 , 4 ]. AKI is defined as a sudden loss of renal function and CKD as decreased function, i.e., glomerular filtration rate (GFR) <60 mL/min/1.73 m 2 , or presence of kidney damage markers for more than 3 months [ 5 , 6 ].…”

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“…The systemic toxicity of the metallic NPs can be diminished by targeting a specific site or by using biodegradable polymers as reduction and functionalizing agents. Metallic NPs may also show toxicity directly through their dissociated ions (24)(25)(26).…”

“…At higher concentration of ROS species, pro-inflammatory signalling pathways such as JNK and NF-κB cascade are activated. Higher ROS concentrations that cause prolonged OS lead to changes in the mitochondrial membrane potential causing cell death (25,(55)(56)(57)(58).…”