Article
Pharmacology & Pharmacy
Yong Fu, Jun Shi, Hong Qian, Chaoyi Qin, Lulu Liu, Jiayu Shen, Hao Ma, Lang Ma, Bin Liao, Yingqiang Guo
Summary: This study investigated the therapeutic effect of peritoneal matrix-loaded pirfenidone nanodroplets (NDs) on myocardial infarction (MI) fibrosis. The results showed that the nanodroplets achieved a slow drug release and inhibited cardiac fibroblasts transformation and collagen synthesis. Combining the peritoneal matrix with pirfenidone nanodroplets showed excellent therapeutic effects on fibrosis in MI rats. This study confirmed the feasibility and synergistic effectiveness of the approach and highlighted the potential application of nanomedicine in other biomedical fields.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Jan Philipp Schuette, Mailin-Christin Manke, Katherina Hemmen, Patrick Muenzer, Barbara F. Schoerg, Gustavo Campos Ramos, Michaela Pogoda, Valerie Dicenta, Sabrina H. L. Hoffmann, Juergen Pinnecker, Ferdinand Kollotzek, Monika Zdanyte, Karin A. L. Mueller, Yogesh Singh, Andreas F. Mack, Bernd Pichler, Florian Lang, Bernhard Nieswandt, Meinrad Gawaz, Katrin G. Heinze, Nicolas Casadei, Oliver Borst
Summary: Platelet-derived miRNAs play a critical role in myocardial inflammation and structural remodeling in response to myocardial ischemia/reperfusion (I/R). In a mouse model with a Dicer gene deletion, disrupted miRNA processing machinery in platelets led to increased myocardial inflammation, impaired angiogenesis, accelerated cardiac fibrosis, and larger infarct size. These findings highlight the importance of platelet-derived miRNA in regulating cellular processes following myocardial I/R.
CIRCULATION RESEARCH
(2023)
Article
Engineering, Environmental
Zhicun Wang, Cheng Hu, Wen Zhang, Wenqi Liu, Ruiqi Dong, Shuyi He, Dongdong Wu, Yunbing Wang, Li Yang
Summary: Injectable hydrogels have the potential to effectively treat myocardial infarction by modulating the microenvironment and function of the heart at different stages, providing therapeutic benefits such as promoting cell proliferation, inhibiting fibrosis, and improving heart function.
CHEMICAL ENGINEERING JOURNAL
(2023)
Article
Biochemistry & Molecular Biology
Cai-Xia Ma, Zhi-Ru Wei, Tong Sun, Ming-Hui Yang, Yu-Qie Sun, Kun-Lun Kai, Jia-Chen Shi, Meng-Jiao Zhou, Zi-Wei Wang, Jing Chen, Wei Li, Tian-Qi Wang, Shan-Feng Zhang, Lixiang Xue, Min Zhang, Qianqian Yin, Ming-Xi Zang
Summary: The transdifferentiation from cardiac fibroblasts to myofibroblasts is a crucial step in the development of cardiac fibrosis. However, the mechanism behind this process is not fully understood. In this study, we identified a novel circular RNA called circ-sh3rf3, which was down-regulated in isoproterenol-treated rat cardiac fibroblasts and cardiomyocytes as well as during fibroblast differentiation into myofibroblasts. We further revealed that circ-sh3rf3 could interact with GATA-4 proteins and regulate the expression of miR-29a, thereby inhibiting fibroblast-myofibroblast differentiation and myocardial fibrosis.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2023)
Article
Immunology
Shiyu Hu, Yang Gao, Rifeng Gao, Yiwen Wang, Yanan Qu, Ji'e Yang, Xiang Wei, Feng Zhang, Junbo Ge
Summary: The selective STING inhibitor H-151 can alleviate myocardial infarction (MI) injury and cardiac fibrosis by inhibiting the type I interferon response triggered by cardiac dsDNA.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Review
Cardiac & Cardiovascular Systems
Stefan Frantz, Moritz Jens Hundertmark, Jeanette Schulz-Menger, Frank Michael Bengel, Johann Bauersachs
Summary: Most patients survive acute myocardial infarction, but the prevalence of heart failure is increasing, leading to economic strain on healthcare systems. Pathological changes in the heart significantly impact patient outcomes. Risk factors like diabetes, chronic obstructive pulmonary disease, and female sex can distinctively shape the progression towards heart failure.
EUROPEAN HEART JOURNAL
(2022)
Article
Cardiac & Cardiovascular Systems
Ryan M. Burke, Ronald A. Dirkx, Pearl Quijada, Janet K. Lighthouse, Amy Mohan, Meghann O'Brien, Wojciech Wojciechowski, Collynn F. Woeller, Richard P. Phipps, Jeffrey D. Alexis, John M. Ashton, Eric M. Small
Summary: Salinomycin as an antifibrotic agent demonstrates potent anti-fibrotic activity in cardiac fibroblasts, prevents cardiac fibrosis and functional decline in mouse models of ischemic and nonischemic heart disease, and inhibits cardiac fibroblast activation by targeting p38/MAPK and Rho signaling. Moreover, salinomycin promotes cardiomyocyte survival and improves coronary vessel density, showing promise for the treatment of heart failure patients.
CIRCULATION RESEARCH
(2021)
Review
Biochemistry & Molecular Biology
Jae-Ho Park, Changwon Kho
Summary: Calcium signaling in the heart is crucial for muscle contraction and electrical signals, with impairment of Ca2+ handling proteins being a key hallmark of heart disease. The discovery of miRNAs as gene regulators has expanded our understanding of cardiac Ca2+ cycling, and there has been significant exploration of their involvement in heart diseases. This review aims to summarize Ca2+ signaling and Ca2+-related miRNAs in cardiac pathologies, as well as discuss the therapeutic potential of targeting these miRNAs for heart disease treatment.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Jing-jing Ji, Ling-lin Qian, Yi Zhu, Yu Jiang, Jia-qi Guo, Ya Wu, Zi-wei Yang, Yu-yu Yao, Gen-shan Ma
Summary: This study found that Serpina3c inhibits the transcriptional activation of ENO1 by regulating the acetylation of Nr4a1, thereby inhibiting glycolysis and reducing fibrosis after myocardial infarction (MI). Serpina3c is a potential target for the prevention and treatment of heart failure after MI.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2022)
Review
Cardiac & Cardiovascular Systems
Chan Wu, Binghong Liu, Ruiying Wang, Gang Li
Summary: Myocardial infarction (MI) is a common cardiovascular disease with high mortality. MiRNAs play a crucial regulatory role in MI, involving mechanisms such as apoptosis, autophagy, proliferation, and inflammation. Furthermore, miRNAs also regulate structural changes after MI, including angiogenesis, myocardial remodeling, and fibrosis.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2022)
Article
Cardiac & Cardiovascular Systems
Yasuhiro Shintani, Takafumi Nakayama, Ayako Masaki, Masashi Yokoi, Kazuaki Wakami, Tsuyoshi Ito, Toshihiko Goto, Tomonori Sugiura, Hiroshi Inagaki, Yoshihiro Seo
Summary: Quantitative pathological findings derived from endomyocardial biopsies, such as collagen area fraction (CAF) and the number of infiltrating CD3(+) cells, are independent predictors of poor clinical outcomes in patients with hypertrophic cardiomyopathy. Cardiomyocyte diameter and nuclear irregularity do not significantly impact the clinical prognosis.
INTERNATIONAL JOURNAL OF CARDIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Xiaoqiong Wei, Song Zou, Zhonghui Xie, Zhen Wang, Nongyu Huang, Zhifu Cen, Yan Hao, Chengxin Zhang, Zhenyu Chen, Fulei Zhao, Zhonglan Hu, Xiu Teng, Yiyue Gui, Xiao Liu, Huaping Zheng, Hong Zhou, Shuwen Chen, Juan Cheng, Fanlian Zeng, Yifan Zhou, Wenling Wu, Jing Hu, Yuquan Wei, Kaijun Cui, Jiong Li
Summary: The study demonstrates the important role of EDIL3 in cardiac remodeling after myocardial infarction. EDIL3 deficiency improves adverse cardiac healing mainly through the mechanism of neutrophil extracellular trap-mediated pro-inflammatory macrophage polarization.
CARDIOVASCULAR RESEARCH
(2022)
Article
Cardiac & Cardiovascular Systems
Xinying Yang, Xiaoyu Du, Ke Ma, Guoqi Li, Zhuohui Liu, Wei Rong, Huangtai Miao, Fuli Zhu, Qinghua Cui, Shaowei Wu, Yulin Li, Jie Du
Summary: This study found that circulating miR-26a-5p, miR-21-5p, and miR-191-5p levels were lower in patients who experienced major adverse cardiovascular events after acute myocardial infarction compared to those who did not. Multivariate conditional logistic regression analysis showed that these miRNAs were significantly inversely associated with incident primary composite outcomes. Combining these miRNAs with B-type natriuretic peptide improved risk scores recommended in the current guidelines.
CANADIAN JOURNAL OF CARDIOLOGY
(2021)
Article
Medicine, Research & Experimental
Yan Wang, Yu Zhang, Jiao Li, Chaofu Li, Ranzun Zhao, Changyin Shen, Weiwei Liu, Jidong Rong, Zhenglong Wang, Junbo Ge, Bei Shi
Summary: In this study, the functional significance of VSIG4 in acute myocardial infarction (AMI) was investigated using VSIG4 knockout and adoptive bone marrow transfer chimeric models. The results showed that VSIG4 promotes scar formation, orchestrates the myocardial inflammatory response, and enhances the production of TGF-beta 1 and IL-10. Additionally, hypoxia was found to induce VSIG4 expression in cultured bone marrow M2 macrophages, leading to the conversion of cardiac fibroblasts to myofibroblasts. These findings highlight the crucial role of VSIG4 in AMI and suggest potential immunomodulatory therapeutic strategies for fibrosis repair after AMI.
Article
Chemistry, Multidisciplinary
Xuehui Zheng, Lingxin Liu, Jing Liu, Chen Zhang, Jie Zhang, Yan Qi, Lin Xie, Chunmei Zhang, Guoqing Yao, Peili Bu
Summary: The study shows that adverse remodeling after myocardial infarction (MI) is associated with heart failure and sudden cardiac death. Fibulin7 (FBLN7) is a critical profibrotic regulator of post-MI cardiac remodeling. FBLN7 binds to the epidermal growth factor receptor (EGFR) and induces autophosphorylation of EGFR, leading to fibroblast-to-myofibroblast transdifferentiation and myocardial fibrosis.