Association of nanoparticles and Nrf2 with various oxidative stress-mediated diseases

Thiruvengadam, Rekha; Venkidasamy, Baskar; Samynathan, Ramkumar; Rajakumar, Govindasamy; Thiruvengadam, Muthu; Kim, Jin Hee

doi:10.1016/j.cbi.2023.110535

Cited by 6 publications

(3 citation statements)

References 247 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This process can be effectively blocked by the use of antioxidants. The epigenetic modifications, including DNA methylation and histone methylation, potentially modulated the expression of Nrf2 [191]. Multiple reports have emerged discussing the indispensable functions of histone-modifying enzymes and DNA methylation patterns in preserving podocyte integrity, particularly in diabetic circumstances [192].…”

Section: Dna Methylationmentioning

confidence: 99%

Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease

Wang,

Zhang

2024

Antioxidants

View full text Add to dashboard Cite

Diabetic kidney disease (DKD) is the principal culprit behind chronic kidney disease (CKD), ultimately developing end-stage renal disease (ESRD) and necessitating costly dialysis or kidney transplantation. The limited therapeutic efficiency among individuals with DKD is a result of our finite understanding of its pathogenesis. DKD is the result of complex interactions between various factors. Oxidative stress is a fundamental factor that can establish a link between hyperglycemia and the vascular complications frequently encountered in diabetes, particularly DKD. It is crucial to recognize the essential and integral role of oxidative stress in the development of diabetic vascular complications, particularly DKD. Hyperglycemia is the primary culprit that can trigger an upsurge in the production of reactive oxygen species (ROS), ultimately sparking oxidative stress. The main endogenous sources of ROS include mitochondrial ROS production, NADPH oxidases (Nox), uncoupled endothelial nitric oxide synthase (eNOS), xanthine oxidase (XO), cytochrome P450 (CYP450), and lipoxygenase. Under persistent high glucose levels, immune cells, the complement system, advanced glycation end products (AGEs), protein kinase C (PKC), polyol pathway, and the hexosamine pathway are activated. Consequently, the oxidant–antioxidant balance within the body is disrupted, which triggers a series of reactions in various downstream pathways, including phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), transforming growth factor beta/p38-mitogen-activated protein kinase (TGF-β/p38-MAPK), nuclear factor kappa B (NF-κB), adenosine monophosphate-activated protein kinase (AMPK), and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling. The disease might persist even if strict glucose control is achieved, which can be attributed to epigenetic modifications. The treatment of DKD remains an unresolved issue. Therefore, reducing ROS is an intriguing therapeutic target. The clinical trials have shown that bardoxolone methyl, a nuclear factor erythroid 2-related factor 2 (Nrf2) activator, blood glucose-lowering drugs, such as sodium-glucose cotransporter 2 inhibitors, and glucagon-like peptide-1 receptor agonists can effectively slow down the progression of DKD by reducing oxidative stress. Other antioxidants, including vitamins, lipoic acid, Nox inhibitors, epigenetic regulators, and complement inhibitors, present a promising therapeutic option for the treatment of DKD. In this review, we conduct a thorough assessment of both preclinical studies and current findings from clinical studies that focus on targeted interventions aimed at manipulating these pathways. We aim to provide a comprehensive overview of the current state of research in this area and identify key areas for future exploration.

show abstract

Section: Dna Methylationmentioning

confidence: 99%

Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease

Wang,

Zhang

2024

Antioxidants

View full text Add to dashboard Cite

show abstract

“…These symptoms can include proteinuria, edema, fatigue, weakness, high blood pressure, and anemia. 139 Early diagnosis and intervention are crucial for effectively managing DN. DN is mainly characterized by chronic inflammation, oxidative stress, and impaired kidney function, resulting in the progressive loss of kidney structure and function.…”

Section: Therapeutic Applicationsmentioning

confidence: 99%

“…Current treatment strategies primarily focus on blood glucose control, blood pressure management, and the use of certain medications to slow disease progression. [137][138][139] However, these approaches may have limitations and may not fully halt the progression of DN.…”

Section: Nephropathymentioning

confidence: 99%