Oxidative Stress and the Kidney: From Physiological Homeostasis to Pathophysiology and Nutraceutical Interventions

Dear Colleagues,

Kidney disease is a worldwide health burden with a high economic cost, with more than one million annual deaths from end-stage renal disease (ESRD). The kidney is the second highest organ consuming oxygen at a resting state, which makes it vulnerable to damage caused by oxidative stress, and several studies have shown that oxidative stress can accelerate kidney disease progression but also many complications such as hypertension, atherosclerosis, inflammation, and anemia.

Regarding physiological conditions in the kidney, the greatest proportion of ATP derives from oxidative phosphorylation (OXPHOS) in the mitochondrial matrix. Mitochondrial homeostasis is vital to maintain normal kidney function, as mitochondrial dysfunction not only contributes to energy deficiency but also leads to disruption of cellular homeostasis and renal function. The main phenomenon of mitochondrial dysfunction is the excessive generation of reactive oxygen species (ROS), which plays a key role in cell injury and kidney diseases.

Oxidative stress does not merely accompany CKD but actively perpetuates its progression. Mitochondrial dysfunction, characterized by impaired biogenesis, disrupted dynamics, and defective mitophagy, drives sustained ROS generation and activates profibrotic and inflammatory signaling cascades, including NF-κB and the NLRP3 inflammasome.

Levels of ROS are maintained as a balance between oxidants and antioxidants; however, antioxidant defense mechanisms have been shown to be compromised in patients with renal dysfunction.

Current therapies using commercially available drugs, such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and calcium channel blockers, generally only delay the progression of CKD.

Natural compounds can modulate several pathways involved in CKD progression, including the epithelial-to-mesenchymal transition (EMT) via antioxidant, anti-inflammatory, or anti-fibrotic mechanisms; they also can reduce oxidative stress by promoting mitochondrial biogenetics and energetics, reducing mitochondrial ROS, or enhancing antioxidant gene expression.

Combination treatments of plant extracts with conventional therapies may confer additive or synergistic renoprotective effects; therefore, the aim of recent research is to identify and rigorously test pre-clinically and avoid any toxic outcomes to obtain optimal therapeutic benefit from medicinal plants.

Dr. Daniele La Russa
Dr. Daniela Pellegrino
Guest Editors

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