Article
Plant Sciences
Junxiao Xi, Yuezhao Rong, Zifeng Zhao, Yihai Huang, Pu Wang, Huiling Luan, Yan Xing, Siyuan Li, Jun Liao, Yue Dai, Jingyu Liang, Feihua Wu
Summary: The study found that Scutellarin can protect vascular endothelial cells against high glucose-induced injury by regulating mitophagy, potentially involving the modulation of multiple signaling pathways.
JOURNAL OF ETHNOPHARMACOLOGY
(2021)
Review
Physiology
Kai Qu, Fang Yan, Xian Qin, Kun Zhang, Wen He, Mingqing Dong, Guicheng Wu
Summary: Mitochondria play a crucial role in generating ATP and their dysfunction can lead to various cellular pathologies, including atherosclerosis. Endothelial mitochondrial dysfunction contributes to abnormal endothelial function and the development of atherosclerosis. Risk factors associated with atherosclerosis, such as high glucose levels, hypertension, and diabetes, can induce mitochondrial dysfunction in endothelial cells.
FRONTIERS IN PHYSIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Ying Wang, Yuerong Xu, Wangang Guo, Yexian Fang, Lang Hu, Runze Wang, Ran Zhao, Dong Guo, Bingchao Qi, Gaotong Ren, Jun Ren, Yan Li, Mingming Zhang
Summary: The study reveals the role of Shank3 in cardiac aging and its contribution to mitochondrial dysfunction and cardiac damage. Manipulating Shank3/CaMKII-induced mitophagy inhibition could be a potential therapeutic intervention for aging-related cardiac dysfunctions.
Review
Medicine, Research & Experimental
Yuexian Li, Liangyuan Suo, Zhiling Fu, Guoqing Li, Jin Zhang
Summary: Sepsis is a fatal organ dysfunction caused by a disordered host response to infection. Autophagy plays a critical role in endothelial cell injury, but the specific mechanisms in sepsis are not well understood. Increasing evidence suggests that autophagy is closely linked to endothelial function and may have varying effects in sepsis depending on conditions.
Article
Food Science & Technology
Tingting Yan, Jiyang Chen, Yalin Wang, Yinuo Wang, Yuanqingzhi Zhang, Yan Zhao
Summary: This study investigated the effect of alcohol on mitochondrial function in ALDH2-deficient cells. The results showed that alcohol induced excessive mitochondrial fragmentation and impaired function, leading to increased cytotoxicity. Alcohol also caused calcium influx and activated CaMKII. Inhibition of calcium overload or CaMKII activation improved alcohol-induced mitophagy and cytotoxicity.
FOOD AND CHEMICAL TOXICOLOGY
(2023)
Article
Biotechnology & Applied Microbiology
Jie Xiang, Chunling Zhang, Tietao Di, Lu Chen, Wei Zhao, Lianggang Wei, Shiyong Zhou, Xueli Wu, Gengxin Wang, Yun Zhang
Summary: This study found that Salvianolic acid B (Sal B) could improve diabetes-induced endothelial dysfunction and mitochondrial dysfunction by regulating apoptosis and mitophagy of endothelial cells.
Article
Hematology
Lindsay Canham, Sam Sendac, Mannekomba R. Diagbouga, Elena Wolodimeroff, Daniela Pirri, Blanca Tardajos Ayllon, Shuang Feng, Celine Souilhol, Timothy J. A. Chico, Paul C. Evans, Jovana Serbanovic-Canic
Summary: Hemodynamic wall shear stress (WSS) exerted on the endothelium by flowing blood determines the spatial distribution of atherosclerotic lesions. Disturbed flow (DF) with low WSS promotes atherosclerosis, while unidirectional flow with high WSS is protective. This study investigates the role of EVA1A in WSS-regulated endothelial cell dysfunction.
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
(2023)
Article
Allergy
Yan Zhang, Danh C. Do, Xinyue Hu, Ji Wang, Yilin Zhao, Sumita Mishra, Xin Zhang, Mei Wan, Peisong Gao
Summary: The study identified that cockroach allergen activates autophagy, while inhibition of autophagy can mitigate airway hyperresponsiveness and oxidative stress induced by allergic airway inflammation. Furthermore, the research revealed a pathological feedforward circuit between cockroach allergen-induced ROS and autophagy.
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
(2021)
Review
Pharmacology & Pharmacy
Huxinyue Duan, Qing Zhang, Jia Liu, Ruolan Li, Dan Wang, Wei Peng, Chunjie Wu
Summary: Endothelial cell apoptosis is the initial step in the development of atherosclerosis, with risk factors inducing excessive apoptosis. Natural medicines have great potential in treating atherosclerosis by inhibiting endothelial cell apoptosis.
PHARMACOLOGICAL RESEARCH
(2021)
Review
Pharmacology & Pharmacy
Huxinyue Duan, Qing Zhang, Jia Liu, Ruolan Li, Dan Wang, Wei Peng, Chunjie Wu
Summary: Atherosclerosis, a chronic multifactorial disease, is closely related to cardiovascular diseases and is a major cause of death globally. Endothelial cell apoptosis is believed to be the initial step in atherosclerosis development, and natural medicines have great potential in treating atherosclerosis by inhibiting this process.
PHARMACOLOGICAL RESEARCH
(2021)
Review
Biochemistry & Molecular Biology
Xuelian Li, Xianjie Zhu, Yumiao Wei
Summary: Atherosclerosis is a lipid-driven disease characterized by the imbalance between inflammatory and regressive processes. Recent studies have suggested a link between autophagy and vascular inflammation. This review summarizes the underlying mechanisms associated with different autophagic pathways and NLRP3 inflammasomes in vascular inflammation, aiming to provide additional evidence for atherosclerosis research.
Article
Pharmacology & Pharmacy
Amir Ajoolabady, Yaguang Bi, David J. McClements, Gregory Y. H. Lip, Des R. Richardson, Russel J. Reiter, Daniel J. Klionsky, Jun Ren
Summary: Atherosclerosis is a chronic proinflammatory anomaly that can lead to various cardiovascular diseases. Pharmacotherapies and adjuvants such as melatonin have shown promise in alleviating inflammation and improving the condition of the disease.
PHARMACOLOGICAL RESEARCH
(2022)
Article
Cell Biology
Meng Duan, Hainan Chen, Linjie Yin, Xiao Zhu, Petr Novak, Yuncheng Lv, Guojun Zhao, Kai Yin
Summary: AIBP, a secreted protein, plays a pivotal role in the development of atherosclerosis. This study found that AIBP is abundantly expressed in atherosclerotic lesions and localizes in the inner membrane of mitochondria in macrophages. Deficiency of mitochondrial AIBP promotes atherosclerosis progression by causing metabolic disorders and reducing mitophagy. This leads to M1 proinflammatory macrophage polarization, further contributing to atherosclerosis development.
CELL COMMUNICATION AND SIGNALING
(2022)
Article
Biochemistry & Molecular Biology
Changlin Zhai, Yinggang Sun, Gang Qian, Haihua Pan, Shuoyin Xie, Zhewei Sun, Song Zhang, Huilin Hu
Summary: This study identified the roles of lncRNA AK087124 and miR-224-5p in the pathogenesis of atherosclerosis and elucidated the competitive interaction mechanisms between them, providing potential biomarkers and target molecules for the treatment and diagnosis of atherosclerosis.
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
(2021)
Article
Hematology
Soo-Ho Choi, Colin Agatisa-Boyle, Ayelet Gonen, Alisa Kim, Jungsu Kim, Elena Alekseeva, Sotirios Tsimikas, Yury Miller
Summary: The study found that intracellular AIBP plays a role in regulating autophagy in macrophages exposed to OxLDL, protecting against cell death, and is important in atherosclerotic lesions. Mitochondria-localized AIBP enhances mitophagy and participates in mitochondria quality control, indicating a new mechanism for macrophage protection in atherosclerosis.
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
(2021)