Article
Cell Biology
Xiu Mei Ma, Kang Geng, Betty Yuen-Kwan Law, Peng Wang, Yue Li Pu, Qing Chen, Hui Wen Xu, Xiao Zhen Tan, Zong Zhe Jiang, Yong Xu
Summary: The cytosolic mtDNA-induced cGAS-STING activation plays a critical role in the pathogenesis of obesity-related DCM. Increased mtDNA in the cytosol is a result of excessive mitochondrial ROS production, leading to the activation of the cGAS/STING system and subsequent inflammation and apoptosis. Inhibition or knockdown of STING can effectively block the progression of DCM.
CELL BIOLOGY AND TOXICOLOGY
(2023)
Review
Geriatrics & Gerontology
Xudong Zhang, Jiahui Fan, Huaping Li, Chen Chen, Yan Wang
Summary: CD36, also known as scavenger receptor B2, plays multiple roles in lipid metabolism, inflammatory signaling, oxidative stress, and energy reprogramming. It acts as a receptor that interacts with various ligands and activates specific downstream signaling pathways. CD36 signaling is closely related to diabetic cardiomyopathy, presenting a promising strategy for its treatment based on recent basic research and clinical findings.
Review
Cardiac & Cardiovascular Systems
Jiahan Ke, Jianan Pan, Hao Lin, Jun Gu
Summary: Diabetes mellitus (DM) is a global epidemic that often leads to cardiovascular diseases and death. Diabetic cardiomyopathy (DCM) is a heart dysfunction caused by DM, independent of coronary artery diseases and hypertension. Both type 1 and type 2 DM patients are at a high risk of developing DCM and heart failure. The metabolic disorders of obesity and insulin resistance in type 2 DM lead to dyslipidemia and lipotoxicity, causing damage to organs including the heart. Although various mechanisms have been proposed, it is still not fully understood how lipotoxicity affects cardiac function and how DM induces clinical heart syndrome. In this article, we summarize the latest discoveries on lipid-induced cardiac toxicity in diabetic hearts and discuss the potential therapies and controversies in clinical DCM.
Article
Gastroenterology & Hepatology
Alexandra Griffiths, Jun Wang, Qing Song, Samuel Man Lee, Jose Cordoba-Chacon, Zhenyuan Song
Summary: This study found that ATF4 is a major transcription factor mediating hepatic CD36 expression, and its activation is associated with CD36 upregulation induced by palmitate and endoplasmic reticulum stress. The study further confirmed that the activation of the ATF4-CD36 pathway is involved in palmitate-induced hepatic lipotoxicity.
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
(2023)
Review
Biochemistry & Molecular Biology
Nilanjan Ghosh, Leena Chacko, Hiranmoy Bhattacharya, Jayalakshmi Vallamkondu, Sagnik Nag, Abhijit Dey, Tanushree Karmakar, P. Hemachandra Reddy, Ramesh Kandimalla, Saikat Dewanjee
Summary: Diabetes mellitus (DM) and cardiovascular complications often occur together, creating a challenging situation. The development of diabetic cardiomyopathy (DCM) involves complex pathophysiological pathways at the metabolic and molecular level, leading to structural and functional alterations of the heart. Glucagon-like peptide-1 (GLP-1) analogues and sodium-glucose cotransporter-2 (SGLT-2) inhibitors have shown promising results in improving cardiovascular outcomes in diabetes. This article highlights the pathways contributing to DCM and discusses potential future therapies.
Article
Pharmacology & Pharmacy
Yingchun Shao, Mengmeng Li, Qi Yu, Manyu Gong, Yanying Wang, Xuewen Yang, Liheng Liu, Dongping Liu, Zhongyue Tan, Yuanyuan Zhang, Yunmeng Qu, Haodong Li, Yaqi Wang, Lei Jiao, Ying Zhang
Summary: This study found that CDR1as is upregulated in diabetic cardiomyopathy (DCM), and knockdown of CDR1as can improve apoptosis caused by DCM. Mechanistically, CDR1as activates the Hippo signaling pathway by inhibiting MST1 ubiquitination level. Additionally, ALKBH5 activates FOXO3 through m6A demethylation and is involved in the regulation of CDR1as. Overall, this study reveals the important role of the ALKBH5-FOXO3-CDR1as/Hippo signaling pathway in DCM and provides new insights into the critical role of m6A methylation in DCM.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Fan Ying, Hao Liu, Eva Hoi Ching Tang, Ishan Lakhani, Ningning Liu, Zhengyuan Xia, Shiming Liu
Summary: EP4 deficiency in mice under high-fat diet resulted in cardiac hypertrophy and fibrosis, accompanied by reduced fatty acid uptake and inhibited ATP generation. EP4 tightly regulates the rates of cardiac fatty acid uptake and ATP generation via the FOXO1/CD36 signaling axis.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Article
Biochemistry & Molecular Biology
Yogi Umbarawan, Ryo Kawakami, Mas Rizky A. A. Syamsunarno, Hideru Obinata, Aiko Yamaguchi, Hirofumi Hanaoka, Takako Hishiki, Noriyo Hayakawa, Norimichi Koitabashi, Hiroaki Sunaga, Hiroki Matsui, Masahiko Kurabayashi, Tatsuya Iso
Summary: This study investigated the impact of CD36 knockout on STZ-induced diabetic cardiomyopathy, revealing that CD36KO-STZ hearts exhibited significant abnormalities in energy supply and glycolysis, leading to deteriorated cardiac function.
Article
Medicine, Research & Experimental
Meiling Yan, Lun Li, Qing Wang, Xiaoqi Shao, Qingmao Luo, Suping Liu, Yun Li, Dongwei Wang, Yue Zhang, Hongtao Diao, Xianglu Rong, Jiao Guo
Summary: FTZ improves cardiac function, attenuates heart hypertrophy, improves serum lipid and proinflammatory cytokine levels, and restrains oxidative stress and NLRP3 inflammasome-induced inflammatory activities in diabetic mouse hearts.
BIOMEDICINE & PHARMACOTHERAPY
(2022)
Article
Cardiac & Cardiovascular Systems
Xiaodong Wu, Ting Zhang, Ping Lyu, Mengli Chen, Gehui Ni, Huiling Cheng, Guie Xu, Xinli Li, Lijun Wang, Hongcai Shang
Summary: QLQX attenuates diabetic cardiomyopathy by activating PPAR gamma, reducing hyperglycemia-induced cardiomyocyte apoptosis and protecting mice from cardiac dysfunction and pathological remodeling caused by diabetes.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
Article
Medicine, Research & Experimental
Jiabing Zhan, Kunying Jin, Nan Ding, Yufei Zhou, Guo Hu, Shuai Yuan, Rong Xie, Zheng Wen, Chen Chen, Huaping Li, Dao Wen Wang
Summary: Intensive glycemic control is insufficient for reducing the risk of heart failure in patients with diabetes mellitus. MiR-320 and CD36 mutually enhance each other's expression, forming a positive feedback loop that sustains a hyperlipidemic state in the heart.
MOLECULAR THERAPY-NUCLEIC ACIDS
(2023)
Review
Cell Biology
Qutuba G. Karwi, Qiuyu Sun, Gary D. Lopaschuk
Summary: Diabetes increases cardiac reliance on fatty acids as the major energy source, leading to negative impacts on cardiac function and structure, efficiency, and energy status, while also making the heart more vulnerable to ischemic injury.
Article
Pharmacology & Pharmacy
Veronica F. Salau, Ochuko L. Erukainure, Kolawole A. Olofinsan, Nontokozo Z. Msomi, Olayemi K. Ijomone, Md Shahidul Islam
Summary: This study elucidated the protective effect of ferulic acid on diabetic cardiomyopathy in a rat model of type 2 diabetes. The results showed that ferulic acid effectively improved myocardium structural morphology and reversed the levels and activities of various biomarkers associated with diabetes complications.
FUNDAMENTAL & CLINICAL PHARMACOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Chaoyang Liu, Yuehu Han, Xiaoming Gu, Man Li, Yanyan Du, Na Feng, Juan Li, Shumiao Zhang, Leonid N. Maslov, Guoen Wang, Jianming Pei, Feng Fu, Mingge Ding
Summary: This study demonstrated that paeonol protects against mitochondrial disorders and diabetic cardiomyopathy by promoting Opa1-mediated mitochondrial fusion, inhibiting oxidative stress, and activating Stat3 and CK2 alpha signaling pathways. Paeonol's interaction with CK2 alpha restores kinase activity, increasing Jak2-Stat3 phosphorylation and enhancing Opa1 transcriptional expression, providing a promising strategy for DCM treatment.
Article
Medicine, Research & Experimental
Fatemeh Yarmohammadi, A. Wallace Hayes, Gholamreza Karimi
Summary: Cardiac lipotoxicity is the harmful effects of excess lipid deposition in cardiomyocytes, resulting in changes in cardiac structure and function. Dysfunction in the heart is associated with abnormal lipid metabolism, potentially causing cardiomyocyte distress and subsequent contractile dysfunction. Various compounds have been researched for their protective effects against lipotoxicity progression in the heart, involving mechanisms such as improvement of calcium homeostasis, lipid metabolism, and mitochondrial dysfunction.
BIOMEDICINE & PHARMACOTHERAPY
(2022)
