Article
Medicine, Research & Experimental
Jian-Kui Du, Qing Yu, Yu-Jian Liu, Shu-Fang Du, Li-Yang Huang, Dan-Hong Xu, Xin Ni, Xiao-Yan Zhu
Summary: The study reveals the role of KLK8 in diabetic cardiomyopathy, with KLK8 deficiency attenuating cardiac fibrosis while KLK8 overexpression inducing EndMT. This provides a new direction for therapeutic strategies for diabetic cardiomyopathy.
Article
Immunology
Lifang Chen, Guan Wang, Jianyu He, Xin Yang, Zihan Zheng, Ying Deng, Yizhen Liu, Danli Chen, Rong Lin, Weirong Wang
Summary: The study reveals that SIRT6 inhibits EndMT in vascular endothelial cells by attenuating the inflammatory response. Knockout of endothelium-specific SIRT6 promotes EndMT and the expression of proinflammatory cytokines in mice carotid arteries. These findings highlight the significance of SIRT6 in cardiovascular diseases.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Shaohua Zhang, Yan Li, Xiuzhen Huang, Kuo Liu, Qing-Dong Wang, Alex F. Chen, Kun Sun, Kathy O. Lui, Bin Zhou
Summary: The study reveals that during cardiac development, cardiac ECs can transdifferentiate into mesenchymal cells through EndoMT but do not contribute to myofibroblasts or express known mesenchymal genes transiently during fibrosis in the adult heart. Resident fibroblasts are the major contributors to cardiac fibrosis by activating mesenchymal gene expression.
Article
Chemistry, Medicinal
Xingxing Chen, Xue Xia, Tiancheng Dong, Zhiwei Lin, Leilei Du, Hao Zhou
Summary: The study investigated the potential impact of TMZ on cardiac fibrosis by inhibiting NOX2-mediated EndMT. Results showed that TMZ treatment mitigated cardiac fibrosis and improved left ventricular dysfunction by suppressing NOX activity and EndMT. The study suggests that TMZ may play a role in preventing ISO-induced cardiac fibrosis through the NOX2/NF-Kappa B/Snail pathway.
DRUG DESIGN DEVELOPMENT AND THERAPY
(2022)
Article
Cell Biology
Jingjing Tian, Mingjun Zhang, Mengying Suo, Dian Liu, Xuyang Wang, Ming Liu, Jinyu Pan, Tao Jin, Fengshuang An
Summary: The study found that the SGLT2 inhibitor dapagliflozin (DAPA) protects against diabetic cardiomyopathy (DCM) and myocardial fibrosis by suppressing fibroblast activation and endothelial-to-mesenchymal transition (EndMT) through the AMPK alpha-mediated inhibition of the TGF-beta/Smad signaling pathway.
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2021)
Article
Biochemistry & Molecular Biology
Pei-Shan Tsai, Chen-Yuan Chiu, Meei-Ling Sheu, Ching-Yao Yang, Kuo-Cheng Lan, Shing-Hwa Liu
Summary: The study found that AGEs can induce EndMT in islet endothelial cells and lead to islet fibrosis in diabetic mice. This suggests that AGE-induced EndMT may contribute to islet fibrosis in diabetes.
CHEMICO-BIOLOGICAL INTERACTIONS
(2021)
Article
Biochemistry & Molecular Biology
Ruth A. Kelly, Kristin M. Perkumas, Matthew Campbell, G. Jane Farrar, W. Daniel Stamer, Pete Humphries, Jeffrey O'Callaghan, Colm J. O'Brien
Summary: This study found that glaucomatous Schlemm's canal endothelial cells (gSCECs) exhibit a stiffer and more fibrotic phenotype compared to healthy SCECs. gSCECs expressed higher levels of fibrotic markers and increased protein expression of TGF beta-2, a driver of fibrosis. Additionally, gSCECs were larger in size, proliferated and migrated at a higher rate, and showed reduced mitochondrial activity compared to healthy SCECs.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Nina P. Jordan, Samuel J. Tingle, Victoria G. Shuttleworth, Katie Cooke, Rachael E. Redgrave, Esha Singh, Emily K. Glover, Hafiza B. Ahmad Tajuddin, John A. Kirby, Helen M. Arthur, Chris Ward, Neil S. Sheerin, Simi Ali
Summary: The down-regulation of miR-126-3p is associated with EndMT, with its over-expression preventing the process and maintaining endothelial characteristics while repressing fibronectin expression. Lineage tracing in cardiac and kidney fibrosis models revealed that a significant subpopulation of endothelial-derived cells undergo EndMT and express mesenchymal markers. MiR-126-3p expression is restricted to endothelial cells and down-regulated in fibrotic kidney and heart tissue, making it a potential target for miRNA-based therapeutics in fibrotic organs.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Cardiac & Cardiovascular Systems
Eric Wang, Shali Chen, Honglin Wang, Tori Chen, Subrata Chakrabarti
Summary: This study confirms the occurrence of EndMT in human hearts during DCM and its correlation with changes in relevant ncRNAs. It further suggests that there may be an interplay between DNA methylation and certain ncRNAs involved in the regulation of EndMT that contribute to the observed changes in ncRNA expression.
CARDIOVASCULAR DIABETOLOGY
(2023)
Review
Biochemistry & Molecular Biology
Weiming Zhao, Lan Wang, Yaxuan Wang, Hongmei Yuan, Mengxia Zhao, Hui Lian, Shuaichen Ma, Kai Xu, Zhongzheng Li, Guoying Yu
Summary: The pathological features of pulmonary fibrosis (PF) involve abnormal activation and proliferation of myofibroblasts as well as excessive deposition of extracellular matrix (ECM). Recent studies have emphasized the crucial role of endothelial cells in the development of PF, with 16% of fibroblasts in fibrotic mice lung tissue being derived from endothelial cells. The endothelial cells undergo endothelial-mesenchymal transition (E(nd)MT), leading to excessive proliferation of endothelial-derived mesenchymal cells, fibroblast accumulation, and ECM deposition.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Pharmacology & Pharmacy
Wu Luo, Gaojun Wu, Xiaojun Chen, Qiuyan Zhang, Chunpeng Zou, Jun Wang, Jun Liu, Nipon Chattipakorn, Yi Wang, Guang Liang
Summary: The expression of MyD88 protein was found to be increased in the hearts of diabetic mice. Inhibition of MyD88 through siRNA or small-molecular inhibitor markedly reduced inflammatory response and associated cell signaling pathway activation under high glucose conditions. Furthermore, pharmacological inhibition of MyD88 showed anti-inflammatory, anti-hypertrophic, and anti-fibrotic effects in diabetic mouse hearts. These findings indicate that MyD88 may serve as a potential therapeutic target for diabetic cardiomyopathy.
BIOCHEMICAL PHARMACOLOGY
(2022)
Article
Cell Biology
Bai Ruan, Juan-Li Duan, Hao Xu, Kai-Shan Tao, Hua Han, Guo-Rui Dou, Lin Wang
Summary: Liver sinusoidal endothelial cells undergo partial endothelial mesenchymal transition during liver fibrosis, leading to increased extracellular matrix production without activating cell mobility. Targeting this transitional process may be valuable for antifibrotic treatment of liver fibrosis.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Mingchuan Liu, Tingwei Peng, Lang Hu, Min Wang, Dong Guo, Bingchao Qi, Gaotong Ren, Di Wang, Yunqing Li, Liqiang Song, Jianqiang Hu, Yan Li
Summary: This study found that CD147 plays a pivotal role in diabetic cardiac fibrosis, promoting the development of cardiac fibrosis. This discovery may contribute to the future development of CD147-based therapeutic strategies for diabetic cardiomyopathy.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
(2023)
Review
Cell Biology
Ying Chen, Hang Zou, Hongwei Lu, Hong Xiang, Shuhua Chen
Summary: Renal fibrosis is a significant pathological feature of diabetic kidney disease and can eventually lead to renal failure. It is important to understand its mechanism and develop targeted therapies. Recent studies have shown that endothelial-mesenchymal transition (EndMT) plays a crucial role in renal fibrosis.
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Jian-An Pan, Hui Zhang, Hao Lin, Lin Gao, Hui-Li Zhang, Jun-Feng Zhang, Chang-Qian Wang, Jun Gu
Summary: The study revealed the protective role of irisin in EndMT and perivascular fibrosis in the cardiac microenvironment in a mouse DIC model, potentially reversing ROS accumulation and autophagy disorders by regulating UCP2. Irisin was found to be mainly secreted by cardiomyocytes and had a paracrine protective effect on endothelial cells. This study provides a novel perspective on the pathogenesis and potential treatment of DIC.