Article
Cardiac & Cardiovascular Systems
Masum M. Mia, Dasan Mary Cibi, Siti Aishah Binte Abdul Ghani, Anamika Singh, Nicole Tee, Viswanathan Sivakumar, Hanumakumar Bogireddi, Stuart A. Cook, Junhao Mao, Manvendra K. Singh
Summary: Yap/Taz play an important regulatory role in MI-induced cardiac fibrosis by controlling fibroblast proliferation, transdifferentiation into myofibroblasts, and fibroinflammatory program.
CARDIOVASCULAR RESEARCH
(2022)
Review
Cell Biology
Yifang Xie, Jiandong Liu, Li Qian
Summary: The adult human heart has limited regenerative capacity. Direct cardiac reprogramming, which converts cardiac fibroblast into functional cardiomyocyte-like cells, holds great promise for heart regeneration. Significant progress has been made in improving reprogramming efficiency and understanding the underlying molecular mechanisms.
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
(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)
Review
Biotechnology & Applied Microbiology
Wangping Chen, Weihua Bian, Yang Zhou, Jianyi Zhang
Summary: The loss of cardiomyocytes in acute myocardial infarction cannot be effectively replaced by limited regenerative capacity of adult mammalian hearts. Cardiac fibroblasts play a crucial role in fibrosis after MI and may hold potential for reprogramming into cardiomyocytes. Further research is needed to explore the potential of cardiac fibroblasts in improving cardiac performance in injured hearts.
FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
(2021)
Review
Cell Biology
Young-Jae Nam
Summary: Loss of cardiac muscle after injury is replaced by fibrosis, and directly reprogramming fibroblasts into induced cardiomyocyte-like cells is an attractive regenerative approach. However, its translation into clinical practice still faces challenges.
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
(2022)
Article
Immunology
Elena de Dios, Cesar Rios-Navarro, Nerea Perez-Sole, Jose Gavara, Victor Marcos-Garces, Maria J. Forteza, Ricardo Oltra, Jose M. Vila, Francisco J. Chorro, Vicente Bodi
Summary: Lymphopenia after ST-segment elevation myocardial infarction (STEMI) is associated with adverse cardiac consequences and poor prognosis. Increased expression of regulatory T cell and immune checkpoint genes CD25, CD69, PD-1, and CTLA-4 following STEMI correlates with better short- and long-term cardiac structure and function, with CD25 potentially predicting the extent of infarction size after one week.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Article
Multidisciplinary Sciences
Dashuai Zhu, Zhenhua Li, Ke Huang, Thomas G. Caranasos, Joseph S. Rossi, Ke Cheng
Summary: Intrapericardial injection is established as a safe and effective method for delivering therapeutic-bearing hydrogels to the heart, promoting cardiac repair.
NATURE COMMUNICATIONS
(2021)
Article
Biochemistry & Molecular Biology
Di Wang, Yaping Zhang, Tianbao Ye, Runlei Zhang, Lili Zhang, Dongmei Shi, Taixi Li, Guofang Xia, Kaifan Niu, Zhe Zhao, Yu Chen, Weijun Pan, Liang Liu, Xian Jin, Chengxing Shen
Summary: Cardiac fibroblasts play a crucial role in scar formation and cardiac repair after myocardial infarction (MI). The extracellular matrix protein CTHRC1 is involved in vascular remodeling, bone formation, and tumor progression. However, the role and mechanism of CTHRC1 in post-MI wound repair are not fully understood.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
(2023)
Article
Multidisciplinary Sciences
Sarah-Lena Puhl, Michael Hilby, Michael Kohlhaas, Linus M. Keidel, Yvonne Jansen, Michael Hristov, Jakob Schindler, Christoph Maack, Sabine Steffens
Summary: Deficiency of GPR55 affects cardiac physiology and post-MI inflammation, leading to maladaptive cardiac remodeling.
SCIENTIFIC REPORTS
(2021)
Article
Cardiac & Cardiovascular Systems
Yuxia Li, Chaoyang Li, Qianglin Liu, Leshan Wang, Adam X. Bao, Jangwook P. Jung, Sanjeev Dodlapati, Jiangwen Sun, Peidong Gao, Xujia Zhang, Joseph Francis, Jeffery D. Molkentin, Xing Fu
Summary: The deletion of Acta2 does not prevent myofibroblast differentiation in cardiac fibroblasts or affect post-MI cardiac repair. The increased expression and stress fiber formation of non-SM alpha A actin isoforms compensate for the loss of Acta2 in cardiac myofibroblasts.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Zhi-Teng Chen, Qing-Yuan Gao, Mao-Xiong Wu, Meng Wang, Run-Lu Sun, Yuan Jiang, Qi Guo, Da-Chuan Guo, Chi-Yu Liu, Si-Xu Chen, Xiao Liu, Jing-Feng Wang, Hai-Feng Zhang, Yang-Xin Chen
Summary: The study demonstrated the significant role of glycolysis in cardiac fibrosis post-myocardial infarction, with glycolysis inhibition showing potential in reducing cardiac fibroblast activation and fibrosis.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
Review
Cardiac & Cardiovascular Systems
Ruoshui Li, Nikolaos G. Frangogiannis
Summary: Integrins, a family of surface receptors, play a role in sensing mechanical stress and changes in the matrix environment, and are involved in the regulation of fibrosis. In myocardial fibrosis, integrins are implicated in fibrogenic conversion of cardiac fibroblasts and may mediate recruitment and activation of fibrogenic macrophages. The role of integrins in cardiac fibrosis is dependent on the underlying pathologic condition and further research is needed to fully understand their involvement.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2022)
Article
Multidisciplinary Sciences
Xiaoxue Ma, Qingshu Meng, Shiyu Gong, Shanshan Shi, Xiaoting Liang, Fang Lin, Li Gong, Xuan Liu, Yinzhen Li, Mimi Li, Lu Wei, Wei Han, Leng Gao, Zhongmin Liu, Xiaohui Zhou
Summary: Excessive and chronic inflammation after myocardial infarction (MI) causes heart failure through cardiac fibrosis and ventricular remodeling. IL-27, mainly produced by cardiac macrophages, is found to be associated with aggravated fibrosis and cardiac dysfunction post MI. IL-27 activates the JAK/STAT signaling pathway in cardiac fibroblasts (CFs) and promotes their proliferation, migration, and extracellular matrix (ECM) production induced by angiotensin II (Ang II).These findings suggest that IL-27 plays a critical role in chronic inflammation-mediated ventricular remodeling and fibrosis.
Article
Cardiac & Cardiovascular Systems
Yashu Kuang, Xiaolin Li, Xiuxiang Liu, Lu Wei, Xiaoli Chen, Jie Liu, Tao Zhuang, Jingjiang Pi, Yanfang Wang, Chenying Zhu, Xin Gong, Hao Hu, Zuoren Yu, Jiming Li, Ping Yu, Huimin Fan, Yuzhen Zhang, Zhongmin Liu, Lin Zhang
Summary: Loss of endothelial S1pr1 exacerbates post-MI cardiac remodelling and worsens cardiac dysfunction by reducing reparative macrophage accumulation. Activation of S1pr1 enhances Ly6c(low) macrophage proliferation and ameliorates cardiac remodelling after MI through the ERK/CSF1 pathway.
CARDIOVASCULAR RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Chaoyang Li, Jiangwen Sun, Qianglin Liu, Sanjeeva Dodlapati, Hao Ming, Leshan Wang, Yuxia Li, Rui Li, Zongliang Jiang, Joseph Francis, Xing Fu
Summary: After myocardial infarction, cardiac fibroblasts undergo different differentiation states with distinct gene expression profiles, and the mechanisms underlying gene expression changes during activation and differentiation events remain unclear. The study utilized RNA-seq and ATAC-seq to analyze gene expression and chromatin accessibility in mouse cardiac fibroblasts from uninjured and infarcted myocardium, identifying transcription factors that may contribute to differential gene expression between different fibroblast states.
