Article
Cardiac & Cardiovascular Systems
Bastian Bruns, Ricarda Daub, Thomas Schmitz, Maria Hamze-Sinno, Sebastian Spaich, Matthias Dewenter, Chrysovalandis Schwale, Peter Gass, Miriam Vogt, Hugo Katus, Wolfgang Herzog, Hans-Christoph Friederich, Norbert Frey, Jobst-Hendrik Schultz, Johannes Backs
Summary: Deficient central MR/GR signaling may contribute to poor outcomes in patients with depression after myocardial infarction (MI), possibly explaining the lack of effectiveness of antidepressant treatment.
BASIC RESEARCH IN CARDIOLOGY
(2022)
Article
Engineering, Environmental
Xiaopei Li, Peng Lu, Zhaoyang Liu, Ziang Wen, Xiangyu Li, Chufan Wang, Wanjun Jin, Bin Zhou, Ningping Huang, Meijuan Song, Xiaowei Wang
Summary: In this study, an anisotropic hydrogel was developed by incorporating polydopamine-reduced graphene oxide-ferric oxide nanohybrids into gelatin methacrylate hydrogels under a direct current-driven magnetic field. Cardiomyocytes cultured on anisotropic hydrogels demonstrated oriented growth and exhibited symmetrical contraction-relaxation behaviors. Both external electrical and alternating magnetic field stimulations enhanced sarcomere functionality, gap junction protein expression, and electrophysiological activities in cardiomyocytes within the anisotropic hydrogel group. In an acute myocardial infarction rat model, the application of the anisotropic hydrogel patch significantly improved cardiac function, mitigated adverse left ventricular dilation and remodeling, reduced infarct size, increased left ventricular wall thickness, promoted angiomyogenesis, and preserved the structural and connected features between cardiomyocytes. The findings highlight the potential of electromagnetic, conductive, and anisotropic gelatin methacrylate-based hydrogels as scaffolds for mimicking the natural functional myocardium layer and developing effective cardiac patches.
CHEMICAL ENGINEERING JOURNAL
(2023)
Article
Cell Biology
Changjun Luo, Si Xiong, Yiteng Huang, Ming Deng, Jing Zhang, Jianlin Chen, Rongfeng Yang, Xiao Ke
Summary: Ischemia/reperfusion-mediated myocardial infarction is a major factor in ischemic heart disease, and key long non-coding RNAs like Gm18840 that are dysregulated during this process have been identified. Gm18840 is upregulated after heart attack and promotes apoptosis in myocardial cells through direct transcriptional regulation of essential genes.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Peripheral Vascular Disease
Fabrizio Buffolo, Martina Tetti, Paolo Mulatero, Silvia Monticone
Summary: In addition to its role in regulating water, sodium, and potassium levels, aldosterone also has an impact on various physiological and pathological processes in the cardiovascular system. High levels of aldosterone are associated with increased risk of cardiovascular events and mortality, while mineralocorticoid receptor antagonists can reduce this risk.
Article
Environmental Sciences
Hang Xu, Na Yang, Bao-Yan Wang, Lin Zhou, Li-Li Xu, Yan Chen, Dong-Jin Wang, Wei-Hong Ge
Summary: This study found that PAGln is upregulated in CAD patients and MI mice, and it may be an independent risk factor for CAD. PAGln pretreatment enhances MI-induced myocardial injury and cardiac fibrosis, possibly through activating GPCR signaling and interacting with β1-AR.
ENVIRONMENTAL TOXICOLOGY
(2023)
Article
Medicine, Research & Experimental
Yuanlong Li, Ming Yang, Jing Tan, Conghui Shen, Shijie Deng, Xinlu Fu, Saifei Gao, Hui Li, Xiaoxue Zhang, Weibin Cai
Summary: The study identifies ACSL1 as a potential factor responsible for the loss of myocardial regenerative potential starting at P7 in mice. Inhibition of ACSL1 effectively promotes myocardial repair after myocardial infarction (MI) in mice.
Article
Cell Biology
Jun Lin, Qinfeng Li, Tingting Jin, Jiacheng Wang, Yingchao Gong, Qingbo Lv, Meihui Wang, Jiawen Chen, Min Shang, Yanbo Zhao, Guosheng Fu
Summary: IL-1R2 plays a protective role in myocardial I/R injury by protecting cardiomyocytes from apoptosis. Overexpression of IL-1R2 can protect cardiomyocytes from apoptosis by reducing the expression of IL-17RA.
CELL DEATH & DISEASE
(2022)
Article
Cardiac & Cardiovascular Systems
Alexander Young, Leigh A. Bradley, Elizabeth Farrar, Helen O. Bilcheck, Svyatoslav Tkachenko, Jeffrey J. Saucerman, Stefan Bekiranov, Matthew J. Wolf
Summary: Inhibition of DYRK1a improves cardiac function and promotes cycling cardiomyocytes after myocardial infarction, suggesting it as a potential therapeutic target for treating MI.
CIRCULATION RESEARCH
(2022)
Review
Cell Biology
Toshiyuki Ko, Seitaro Nomura
Summary: This review summarizes recent studies on manipulating cardiomyocyte plasticity using various approaches such as stem cell differentiation, reprogramming, and reactivation of proliferation as potential treatments for heart disease.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Jiyoung Bae, Rebecca J. Salamon, Emma B. Brandt, Wyatt G. Paltzer, Ziheng Zhang, Emily C. Britt, Timothy A. Hacker, Jing Fan, Ahmed I. Mahmoud
Summary: The study demonstrates that inhibiting succinate and SDH can promote cardiomyocyte proliferation, heart regeneration, and revascularization, with a strong regenerative response observed in adult mouse hearts after myocardial infarction injury. The results suggest a potentially important new therapeutic approach for human heart failure.
Article
Pharmacology & Pharmacy
Zhiyu He, Xiaojun Zeng, Deke Zhou, Peiying Liu, Dunzheng Han, Lingling Xu, Tong Bu, Jinping Wang, Mengmeng Ke, Xiudi Pan, Yipeng Du, Hao Xue, Dongfeng Lu, Bihui Luo
Summary: This study identifies the novel ability of lncRNA Chaer in regulating cardiomyocyte apoptosis by promoting phosphorylation of AMPK in acute myocardial infarction.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Pharmacology & Pharmacy
Evelyne J. Demkes, Steven Wenker, Max J. M. Silvis, Martijn M. J. van Nieuwburg, M. Joyce Visser, Marlijn S. Jansen, Maike A. D. Brans, Evelyn Velema, Joost P. G. Sluijter, Imo E. Hoefer, Dominique P. V. de Kleijn, Leo Timmers, Saskia C. A. de Jager
Summary: The combined treatment of GLP-1R agonist exenatide and MR antagonist potassium canrenoate did not show beneficial effects on cardiac remodeling nor resulted in functional improvement in small and large animal chronic HF models.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Medicine, Research & Experimental
DruAnne L. Maxwell, Timothy D. Bryson, David Taube, Jiang Xu, Edward Peterson, Pamela Harding
Summary: Overexpression of the PGE2 EP3 receptor decreases cardiac function, especially after myocardial infarction. In addition, overexpression of EP3 leads to cardiac hypertrophy, increased collagen fraction, and inflammatory cell infiltration. These findings highlight the importance of EP3 in cardiac diseases.
Article
Biochemistry & Molecular Biology
Yingjie Xu, Zengxiang Dong, Rongzhen Zhang, Zeng Wang, Yuanqi Shi, Mingyu Liu, Jiemei Yang, Tao Yang, Runtong Zhang, Tengyu Wang, Jingyu Zhang, Yu Zhang, Fei Xiang, Yingjun Han, Jiawen Wu, Zhihan Miao, Qiuyu Chen, Qi Li, Zeyao Wang, Ye Tian, Yuanyuan Guo
Summary: Myocardial infarction (MI) is lethal due to acute ischemia and hypoxia, leading to cardiac tissue apoptosis. In this study, we investigated the role of sonodynamic therapy (SDT) in reducing MI-induced cardiomyocyte apoptosis by activating the autophagy pathway. Our results show that SDT improves cardiac function and reduces MI-induced cardiomyocyte apoptosis by enhancing autophagy. Furthermore, we found that the protective effect of SDT is mediated by the activation of MHRT-mediated autophagy. Therefore, SDT may be a potential method for the treatment of post-myocardial infarction heart failure.
FREE RADICAL BIOLOGY AND MEDICINE
(2023)
Article
Cardiac & Cardiovascular Systems
Liangpeng Li, Wenbin Fu, Xue Gong, Zhi Chen, Luxun Tang, Dezhong Yang, Qiao Liao, Xuewei Xia, Hao Wu, Chao Liu, Miao Tian, Andi Zeng, Lin Zhou, Pedro A. Jose, Ken Chen, Wei Eric Wang, Chunyu Zeng
Summary: The study aims to investigate the role of GRK4 in the pathogenesis and progression of myocardial infarction (MI). Results showed that GRK4 expression was increased in the heart after MI, and overexpression of GRK4 aggravated cardiac infarction and dysfunction while specific gene knockout ameliorated these effects. GRK4 inhibited autophagy and promoted cardiomyocyte apoptosis, effects mediated by HDAC4 phosphorylation and a decrease in beclin-1 expression, leading to greater impairment of cardiac function in MI patients carrying the GRK4 A486V variant.
EUROPEAN HEART JOURNAL
(2021)