TY - JOUR
T1 - Disturbed Cardiac Metabolism Triggers Atrial Arrhythmogenesis in Diabetes Mellitus
T2 - Energy Substrate Alternate as a Potential Therapeutic Intervention
AU - Lkhagva, Baigalmaa
AU - Lee, Ting Wei
AU - Lin, Yung Kuo
AU - Chen, Yao Chang
AU - Chung, Cheng Chih
AU - Higa, Satoshi
AU - Chen, Yi Jen
N1 - Funding Information:
This work was supported by grants from the Ministry of Science and Technology (MOST110-2811-B-038-522, MOST111-2811-B-038-014, MOST109-2314-B-038-124-MY3, and MOST110-2314-B-038-107-MY3), Taipei Heart Institute from the Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education in Taiwan (DP2-109-21121-01-H-01 and DP2-110-21121-01-H-01).
Publisher Copyright:
© 2022 by the authors.
PY - 2022/9
Y1 - 2022/9
N2 - Atrial fibrillation (AF) is the most common type of sustained arrhythmia in diabetes mellitus (DM). Its morbidity and mortality rates are high, and its prevalence will increase as the population ages. Despite expanding knowledge on the pathophysiological mechanisms of AF, current pharmacological interventions remain unsatisfactory; therefore, novel findings on the underlying mechanism are required. A growing body of evidence suggests that an altered energy metabolism is closely related to atrial arrhythmogenesis, and this finding engenders novel insights into the pathogenesis of the pathophysiology of AF. In this review, we provide comprehensive information on the mechanistic insights into the cardiac energy metabolic changes, altered substrate oxidation rates, and mitochondrial dysfunctions involved in atrial arrhythmogenesis, and suggest a promising advanced new therapeutic approach to treat patients with AF.
AB - Atrial fibrillation (AF) is the most common type of sustained arrhythmia in diabetes mellitus (DM). Its morbidity and mortality rates are high, and its prevalence will increase as the population ages. Despite expanding knowledge on the pathophysiological mechanisms of AF, current pharmacological interventions remain unsatisfactory; therefore, novel findings on the underlying mechanism are required. A growing body of evidence suggests that an altered energy metabolism is closely related to atrial arrhythmogenesis, and this finding engenders novel insights into the pathogenesis of the pathophysiology of AF. In this review, we provide comprehensive information on the mechanistic insights into the cardiac energy metabolic changes, altered substrate oxidation rates, and mitochondrial dysfunctions involved in atrial arrhythmogenesis, and suggest a promising advanced new therapeutic approach to treat patients with AF.
KW - atrial arrhythmogenesis
KW - energy metabolism
KW - fatty acid oxidation
KW - glucose oxidation
KW - ketone body
KW - mitochondria
UR - http://www.scopus.com/inward/record.url?scp=85138319760&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85138319760&partnerID=8YFLogxK
U2 - 10.3390/cells11182915
DO - 10.3390/cells11182915
M3 - Review article
C2 - 36139490
AN - SCOPUS:85138319760
VL - 11
JO - Cells
JF - Cells
IS - 18
M1 - 2915
ER -
