Sirtuins and Vitamin D: Breakthroughs in Combating Oxidative Stress, Cardiovascular, and Neurodegenerative Diseases
August 25, 2024Drug repositioning is emerging as a promising strategy for developing new treatments for neuroinflammatory disorders, which affect approximately 50 million people globally.
The Special Issue 'Marine Anti-inflammatory and Antioxidant Agents 3.0' showcases the potential of marine environments for bioactive compounds that can treat inflammatory diseases sustainably.
Research highlights the potential of sirtuins, particularly SIRT1 and SIRT3, as therapeutic targets for reducing oxidative stress and enhancing cardiovascular health.
While SIRT1 has shown promise, its effectiveness in managing renal fibrosis remains controversial, necessitating further investigation.
A review of SIRT1's biological roles reveals its involvement in lipid metabolism, epithelial-mesenchymal transition, oxidative stress, aging, inflammation, and autophagy in the context of renal fibrosis.
Microglia play a dual role in neuroinflammatory responses, capable of both promoting damage and providing neuroprotection, which is crucial in neurodegenerative disorders.
Neurodegenerative disorders are characterized by the progressive loss of neurons, with their prevalence increasing as the elderly population grows.
Vitamin D and its analogues are being explored as potential treatments for kidney-related diseases due to their anti-inflammatory, antioxidant, and anti-fibrotic properties.
Clinical trials indicate that vitamin D supplementation correlates with improved kidney health by modulating immunity and metabolism.
The findings underscore the importance of personalized medicine approaches in managing cardiovascular health through targeted antioxidant therapies.
The NLRP3 inflammasome has gained attention for its role in promoting neuroinflammation and programmed cell death, emphasizing the importance of inflammation in neurodegenerative diseases.
Oxidative stress is identified as a key factor in neurodegenerative diseases, contributing to synaptic loss and neuronal death.
Summary based on 7 sources