Quercetin activates the Sestrin2/AMPK/SIRT1 axis to improve amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a chronic neurodegenerative disease with poor prognosis. The intricacies surrounding its pathophysiology could partly account for the lack of effective treatment for ALS. Sestrin2 has been reported to improve metabolic, cardiovascular and neurodegenerative diseases, and is involved in the direct and indirect activation of the adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/silent information regulator 1 (SIRT1) axis. Quercetin, as a phytochemical, has considerable biological activities, such as anti-oxidation, anti-inflammation, anti-tumorigenicity, and neuroprotection. Interestingly, quercetin can activate the AMPK/SIRT1 signaling pathway to reduce endoplasmic reticulum stress, and alleviate apoptosis and inflammation. This report examines the molecular relationship between Sestrin2 and AMPK/SIRT1 axis, as well as the main biological functions and research progress of quercetin, together with the correlation between quercetin and Sestrin2/AMPK/SIRT1 axis in neurodegenerative diseases.

Automated summary

This report examines the relationship between Sestrin2 and the AMPK/SIRT1 axis in ALS, a chronic neurodegenerative disease with poor prognosis. It reveals that Sestrin2 can improve metabolic, cardiovascular, and neurodegenerative diseases by activating the AMPK/SIRT1 signaling pathway. In addition, quercetin, a phytochemical, has various biological activities and can activate the AMPK/SIRT1 pathway to reduce endoplasmic reticulum stress, apoptosis, and inflammation.