Amyloid beta 42 disrupts cardiac function in Alzheimer's disease mice via SLC31A1 upregulation-mediated cuproptosis - PubMed
6 hours ago
- #Alzheimer's disease
- #Cuproptosis
- #Cardiac dysfunction
- Amyloid beta 42 (Aβ42) disrupts cardiac function in Alzheimer's disease (AD) mice by upregulating SLC31A1, leading to cuproptosis.
- AD affects not only the brain but also the heart, with epidemiological studies showing impaired cardiac function in AD patients.
- The study used 3 × Tg-AD mouse models and cardiomyocytes to investigate Aβ-induced cardiotoxicity and cuproptosis mechanisms.
- Aβ42 upregulates the copper importer SLC31A1, increasing intracellular copper levels and triggering cuproptosis in cardiomyocytes.
- Cuproptosis leads to mitochondrial dysfunction, reduced ATP production, and increased reactive oxygen species (ROS) levels.
- The copper chelator TTM counteracted Aβ42-induced cardiac dysfunction by inhibiting copper uptake.
- Interfering with SLC31A1 expression in vivo and in vitro partially inhibited cuproptosis and protected cardiac function.
- The findings suggest SLC31A1-mediated cuproptosis as a potential therapeutic target for preserving cardiac health in AD.