Global versus organ‐specific outcome measures in systemic lupus erythematosus: Comment on the articles by Furie et al, Nikpour et al, Wallace et al, Burgos et al, and Ramos‐Casals et al

Monach, Paul A.

doi:10.1002/acr.20053

Cited by 2 publications

(1 citation statement)

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“…49 Low concentrations of complex I subunit and its activity have been found in postoperative PD individual midbrain biopsies and patient-derived platelets. 50 As a result, the experimental shreds of evidence show that aging reduces cellular protective properties by weakening the Nrf2/ARE pathway’s role. Nrf2-Keap1 protein complex functions as a cellular electrochemical detector, regulating antioxidant gene transcription to maintain redox homeostasis.…”

Section: Nrf2 and Mitochondriamentioning

confidence: 99%

Role of Nrf2 Pathway Activation in Neurological Disorder: A Brief Review

Baba

Subramanian

Wahedi

2022

Journal of Pharmacology and Pharmacotherapeutics

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Oxidative stress plays a crucial role in the emergence of numerous neurodegenerative diseases, with protein accumulation and mitochondrial damage, which result in neurological disorders. To minimize oxidative stress, several defensive mechanisms protect nerve cells by releasing antioxidants such as nuclear erythroid factor2 (Nrf2)-Kelch-like ECH-associated protein1 (Keap1) signaling pathway activation has been proved to be a prospective treatment to reduce oxidative stress and neuroinflammation for protection of neurons in a variety of neurological disorders. In this review, we focus beneficial role of Nrf2 in Alzheimer’s and Parkinson’s diseases. Nrf2 is proved to be a master regulator of antioxidants by releasing over 250 cytoprotective genes aimed at oxidative stress and neuroinflammation. In animal studies Nrf2 activation is proved to improve autophagy, mitochondrial biogenesis, and Suppression of inflammatory cytokinin which protects neuronal cells and inhibit progressive neurodegeneration.

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Section: Nrf2 and Mitochondriamentioning

confidence: 99%