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Energy stress induced cardiac autophagy detection via a chronic and dynamic cardiomyocytes-based biosensing platform.
- Source :
-
Biosensors & Bioelectronics . Jan2025, Vol. 267, pN.PAG-N.PAG. 1p. - Publication Year :
- 2025
-
Abstract
- Hypoglycemia is a common complication which occurs during the treatment of diabetes, closely associated with cardiovascular events. A sudden decrease in blood glucose increases the risk of arrhythmia, which can lead to sudden cardiac death. This event is usually accompanied by abnormal electrophysiological activities in cardiomyocytes. However, traditional models do not efficiently reflect real-time cardiomyocyte electrophysiological changes under various glucose deprivation conditions in a large-scale and high-throughput manner. Therefore, we need to develop a new biosensing platform to aid in related scientific research. In this study, a cardiomyocyte-based biosensor was developed for real-time, noninvasive monitoring of the electrophysiological responses of cardiomyocytes under different glucose concentrations. The findings show that low-glucose conditions result in abnormal electrophysiology in cardiomyocytes, but autophagy enables cells to survive this adversity. Inhibition of autophagy exacerbates electrophysiological abnormalities, and long-term glucose starvation causes irreversible damage to cardiomyocytes. The proposed chronic and dynamic cardiomyocyte-based biosensing platform provides a new tool for understanding the effects of hypoglycemia on the in vitro cardiomyocyte-based heart model, revealing that autophagy has the potential to be an alternative treatment for diabetes and hypoglycemia. [ABSTRACT FROM AUTHOR]
- Subjects :
- *BLOOD sugar
*CARDIAC arrest
*CARDIOVASCULAR diseases
*HYPOGLYCEMIA
*AUTOPHAGY
Subjects
Details
- Language :
- English
- ISSN :
- 09565663
- Volume :
- 267
- Database :
- Academic Search Index
- Journal :
- Biosensors & Bioelectronics
- Publication Type :
- Academic Journal
- Accession number :
- 180630052
- Full Text :
- https://doi.org/10.1016/j.bios.2024.116821