期刊：
Journal of Cardiovascular Translational Research,2024年17(6):1219-1228 ISSN：1937-5387
通讯作者：
Li, L
作者机构：
[Xie, Yushu] Univ South China, Hengyang Med Sch, Class Clin Med, Hengyang 421001, Hunan, Peoples R China.;[Xie, Jie] Univ South China, Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;[Li, Liang] Univ South China, Hengyang Med Sch, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Li, L ] U;Univ South China, Hengyang Med Sch, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
关键词：
DNA methylation;Histone methylation;RNA methylation;Ferroptosis
摘要：
Methylation modification is a crucial epigenetic alteration encompassing RNA methylation, DNA methylation, and histone methylation. Ferroptosis represents a newly discovered form of programmed cell death (PCD) in 2012, which is characterized by iron-dependent lipid peroxidation. The comprehensive investigation of ferroptosis is therefore imperative for a more profound comprehension of the pathological and pathophysiological mechanisms implicated in a wide array of diseases. Researches show that methylation modifications can exert either promotive or inhibitory effects on cell ferroptosis. Consequently, this review offers a comprehensive overview of the pivotal role played by methylation in ferroptosis, elucidating its associated factors and underlying mechanisms.
期刊：
Journal of Cardiovascular Translational Research,2024年17(5):1067-1082 ISSN：1937-5387
通讯作者：
Peng, Tianhong;Xie, W;Li, L
作者机构：
[Hou, Qin] Univ South China, Inst Cardiovasc Res,Key Lab Atherosclerol Hunan Pr, Med Res Ctr,Hunan Prov Cooperat Innovat Ctr Mol Ta, Key Lab Atherosclerol Hunan Prov,Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;[Deng, Yunong; Guo, Jiamin; Li, Pin; Yu, Panpan; Xie, Zhongcheng; He, Yinling; Ma, Wentao; Ouyang, Siyu; Tan, Xiaoqian; Lin, Xiaoyan; Liu, Zhiyang] Univ South China, Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;[Zhang, Zhixia; Mo, Qinger; Yu, Jiang; Chen, Dandan] Univ South China, Hengyang Med Sch, Class Clin Med, Hengyang 421001, Hunan, Peoples R China.;[Chen, Xi; Xie, Wei; Peng, Tianhong; Peng, TH] Univ South China, Clin Anat & Reprod Med Applicat Inst, Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;[Li, Liang] Univ South China, Hengyang Med Sch, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Xie, W ; Li, L ; Peng, TH] U;Univ South China, Clin Anat & Reprod Med Applicat Inst, Hengyang Med Sch, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Hengyang Med Sch, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
摘要：
Exosomes, nano-sized small extracellular vesicles, have been shown to serve as mediators between intercellular communications by transferring bioactive molecules, such as non-coding RNA, proteins, and lipids from secretory to recipient cells, modulating a variety of physiological and pathophysiological processes. Recent studies have gradually demonstrated that altered exosome charges may represent a key mechanism driving the pathological process of ferroptosis. This review summarizes the potential mechanisms and signal pathways relevant to ferroptosis and then discusses the roles of exosome in ferroptosis. As well as transporting iron, exosomes may also indirectly convey factors related to ferroptosis. Furthermore, ferroptosis may be transmitted to adjacent cells through exosomes, resulting in cascading effects. It is expected that further research on exosomes will be conducted to explore their potential in ferroptosis and will lead to the creation of new therapeutic avenues for clinical diseases.
摘要：
Acute monocytic leukemia-M5 (AML-M5) remains a challenging disease due to its high morbidity and poor prognosis. In addition to the evidence mentioned earlier, several studies have shown that programmed cell death (PCD) serves a critical function in treatment of AML-M5. However, the role and relationship between ferroptosis and necroptosis in AML-M5 remains unclear. THP-1 cells were mainly treated with Erastin and IMP-366. The changes of ferroptosis and necroptosis levels were detected by CCK-8, western blot, quantitative real-time PCR, and electron microscopy. Flow cytometry was applied to detect the ROS and lipid ROS levels. MDA, 4-HNE, GSH and GSSG were assessed by ELISA kits. Intracellular distribution of FSP1 was studied by immunofluorescent staining and western blot. The addition of the myristoylation inhibitor IMP-366 to erastin-treated acute monocytic leukemia cell line THP-1 cell not only resulted in greater susceptibility to ferroptosis characterized by lipid peroxidation, glutathione (GSH) depletion and mitochondrial shrinkage, as the FSP1 position on membrane was inhibited, but also increased p-RIPK1 and p-MLKL protein expression, as well as a decrease in caspase-8 expression, and triggered the characteristic necroptosis phenomena, including cytoplasmic translucency, mitochondrial swelling, membranous fractures by FSP1 migration into the nucleus via binding importin α2. It is interesting to note that ferroptosis inhibitor fer-1 reversed necroptosis. We demonstrated that inhibition of myristoylation by IMP-366 is capable of switching ferroptosis and ferroptosis-dependent necroptosis in THP-1 cells. In these findings, FSP1-mediated ferroptosis and necroptosis are described as alternative mechanisms of PCD of THP-1 cells, providing potential therapeutic strategies and targets for AML-M5.
作者：
Gan, Tian;Yu, Jianwei;Deng, Zhongliang;He, Jun
期刊：
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY,2024年14:1454076 ISSN：2235-2988
通讯作者：
He, J
作者机构：
[Gan, Tian; He, Jun; He, J] Univ South China, Affiliated Nanhua Hosp, Hengyang Med Sch, Dept Clin Lab, Hengyang, Peoples R China.;[Deng, Zhongliang; Yu, Jianwei] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Dept Publ Hlth,Lab Sci, Hengyang, Hunan, Peoples R China.
通讯机构：
[He, J ] U;Univ South China, Affiliated Nanhua Hosp, Hengyang Med Sch, Dept Clin Lab, Hengyang, Peoples R China.
关键词：
CRISPR/Cas12a;Mycobacterium tuberculosis;enzymatic recombinant isothermal amplification;fluorescence detection;lateral flow test
摘要：
INTRODUCTION: Mycobacterium tuberculosis, the causative agent of human tuberculosis, poses a significant threat to global public health and imposes a considerable burden on the economy. However, existing laboratory diagnostic methods for M. tuberculosis are time-consuming and have limited sensitivity levels. METHODS: The CRISPR/Cas system, commonly known as the "gene scissors", demonstrates remarkable specificity and efficient signal amplification capabilities. Enzymatic recombinase amplification (ERA) was utilized to rapidly amplify trace DNA fragments at a consistent temperature without relying on thermal cyclers. By integrating of CRISPR/Cas12a with ERA, we successfully developed an ERA-CRISPR/Cas12a detection system that enables rapid identification of M. tuberculosis. RESULTS: The sensitivity of the ERA-CRISPR/Cas12a fluorescence and lateral flow systems was 9 copies/μL and 90 copies/μL, respectively. Simultaneously, the detection system exhibited no cross-reactivity with various of respiratory pathogens and non-tuberculosis mycobacteria, demonstrating a specificity of 100%. The positive concordance rate between the ERA-CRISPR/Cas12a fluorescence system and commercial qPCR was 100% in 60 clinical samples. Meanwhile, the lateral flow system showed a positive concordance rate of 93.8% when compared to commercial qPCR. Both methods demonstrated a negative concordance rate of 100%, and the test results can be obtained in 50 min at the earliest. DISCUSSION: The ERA-CRISPR/Cas12a system offers a rapid, sensitive, and specific method that presents a novel approach to laboratory diagnosis of M. tuberculosis.
摘要：
心脏磁共振（Cardiac magnetic resonance， CMR）具有无辐射、多参数、多序列、多平面等优点，能够实现对冠状动脉疾病患者心脏运动及形态功能、血流和灌注等一站式评估。在本文中，我们将简要介绍心脏磁共振的常见序列及模块，并重点介绍各个参数在冠状动脉疾病的诊断、治疗和预后评估等方面的应用。
摘要：
Coronavirus Disease 2019 (COVID-19) is generally susceptible to the population, highly infectious, rapidly transmitted, and highly fatal. There is a lack of specific drugs against the virus at present and vaccination is the most effective strategy to prevent infection. However, studies have found that some groups, particularly patients with diabetes, show varying degrees of weak immune reactivity to various COVID-19 vaccines, resulting in poor preventive efficacy against the novel coronavirus in patients with diabetes. Therefore, in this study, patients with type 2 diabetes mellitus (T2DM) who had weak immune response to the COVID-19 vaccine in recent years were analyzed. This article reviews the phenomenon, preliminary mechanism, and related factors affecting weak vaccine response in patients with T2DM, which is expected to help in the development of new vaccines for high-risk groups for COVID-19.
作者机构：
[Li, Jierong; Zheng, Zhi; Nie, Yali; Tan, Ying; Zheng, Z] Univ South China, Hunan Prov Key Lab Multi & Artificial Intelligence, Hengyang 421001, Peoples R China.;[Li, Jierong; Zheng, Zhi; Nie, Yali; Tan, Ying; Zheng, Z] Univ South China, Inst Cardiovasc Dis, Hengyang 421001, Peoples R China.;[Li, Jierong; Zheng, Zhi; Nie, Yali; Tan, Ying; Zheng, Z] Univ South China, Hengyang Med Sch, Dept Cardiol, Hengyang 421001, Peoples R China.
通讯机构：
[Nie, YL; Zheng, Z ] U;Univ South China, Hunan Prov Key Lab Multi & Artificial Intelligence, Hengyang 421001, Peoples R China.;Univ South China, Inst Cardiovasc Dis, Hengyang 421001, Peoples R China.;Univ South China, Hengyang Med Sch, Dept Cardiol, Hengyang 421001, Peoples R China.
摘要：
Ischemia/reperfusion (I/R) injury following myocardial infarction is a major cause of cardiomyocyte death and impaired cardiac function. Although clinical data show that metformin is effective in repairing cardiac I/R injury, its efficacy is hindered by non-specific targeting during administration, a short half-life, frequent dosing, and potential adverse effects on the liver and kidneys. In recent years, injectable hydrogels have shown substantial potential in overcoming drug delivery challenges and treating myocardial infarction. To this end, we developed a natural polymer hydrogel system comprising methacryloylated chitosan and methacryloylated gelatin modified with polyaniline conductive derivatives. In vitro studies demonstrated that the optimized hydrogel exhibited excellent injectability, biocompatibility, biodegradability, suitable mechanical properties, and electrical conductivity. Incorporating metformin into this hydrogel significantly extended the administration cycle, mitigated mitochondrial damage, decreased abnormal ROS production, and enhanced cardiomyocyte function. Animal experiments indicated that the metformin/hydrogel system reduced arrhythmia incidence, infarct size, and improved cardiac mitochondrial and overall cardiac function, promoting myocardial repair in I/R injury. Overall, the metformin-loaded conductive hydrogel system effectively mitigates mitochondrial oxidative damage and improves cardiomyocyte function, thereby offering a theoretical foundation for the potential application of metformin in cardioprotection.
摘要：
Ovarian cancer is one of the most common malignant tumors in women, and treatment options are limited. Despite efforts to adjust cancer treatment models and develop new methods, including tumor microenvironment (TME) therapy, more theoretical support is needed. Increasing attention is being given to antiangiogenic measures for TME treatment. Another important concept in ovarian cancer TME is angiogenesis, where tumor cells obtain nutrients and oxygen from surrounding tissues through blood vessels to support further expansion and metastasis. Many neovascularization signaling pathways become imbalanced and hyperactive during this process. Inhibiting these abnormal pathways can yield ideal therapeutic effects in patients, even by reversing drug resistance. However, these deep TME signaling pathways often exhibit crosstalk and correlation. Understanding these interactions may be an important strategy for further treating ovarian cancer. This review summarizes the latest progress and therapeutic strategies for these angiogenic signaling pathways in ovarian cancer.
期刊：
Journal of the American Heart Association,2024年13(21):e036350
通讯作者：
Chang, MZ;Ruan, ZF
作者机构：
[Yuan, Junjie; Chen, Qiong; Qiu, Zhongming] Army Med Univ, Mil Med Univ 3, Xinqiao Hosp, Dept Neurol, Chongqing, Peoples R China.;[Yuan, Junjie; Chen, Qiong; Qiu, Zhongming] Army Med Univ, Mil Med Univ 3, Affiliated Hosp 2, Chongqing, Peoples R China.;[Yuan, Junjie] Gen Hosp Southern Theatre Command PLA, Dept Crit Care Med, Guangzhou, Peoples R China.;[Yuan, Junjie] Gen Hosp Southern Theatre Command PLA, Dept Anesthesiol, Guangzhou, Peoples R China.;[Yuan, Junjie; Wu, Fengfu] 925th Hosp Chinese Peoples Liberat Army, Dept Neurol, Guiyang, Peoples R China.
通讯机构：
[Ruan, ZF ] U;[Chang, MZ ] N;Northwest Univ, Xian Hosp 3, Affiliated Hosp, Dept Neurol, 10 East Sect Fengcheng 3rd Rd, Xian 710000, Peoples R China.;Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Neurol, 69 Chuanshan Ave, Hengyang 421001, Peoples R China.
摘要：
BACKGROUND: First-pass successful reperfusion (FPSR), defined as a successful/complete reperfusion achieved after a single thrombectomy pass, is predictive of favorable outcome in patients with acute ischemic stroke with large-vessel occlusion. It is unknown whether intravenous tirofiban is effective in increasing the rate of FPSR in acute anterior large-vessel occlusion stroke. METHODS AND RESULTS: Patients who had acute large-vessel occlusion stroke presenting within 24 hours and underwent endovascular thrombectomy were analyzed from the RESCUE BT (Intravenous Tirofiban for Patients With Large Vessel Occlusion Stroke) clinical trial, of which the main analysis was neutral. The RESCUE BT trial randomized patients to receive either intravenous tirofiban or placebo before endovascular thrombectomy. The primary end point was FPSR, defined as successful reperfusion (extended thrombolysis in cerebral infarction scale 2b50, 2c, or 3) at first thrombectomy attempt. A modified Poisson regression analysis assessed the association between intravenous tirofiban treatment and FPSR. Of 948 enrolled patients, 463 patients were randomized to the tirofiban group and 485 to the placebo group. The mean age was 67 years, and 41.0% of the patients were women. FPSR was achieved more often in the tirofiban group (30.5% versus 23.5%; adjusted risk ratio, 1.24 [95% CI, 1.01-1.51]; P=0.04). FPSR was associated with a favorable shift to lower modified Rankin Scale disability levels at 90 days (common odds ratio, 1.42 [95% CI, 1.08-1.86]; P=0.01). CONCLUSIONS: In this post hoc analysis of the RESCUE BT trial, treatment with intravenous tirofiban before endovascular thrombectomy was associated with increased FPSR in patients with acute ischemic stroke due to large-vessel occlusion in the anterior circulation. FPSR was associated with reduced 90-day levels of disability. REGISTRATION: URL: http://chictr.org; Unique Identifier: ChiCTR-INR-17014167.
摘要：
Tripartite-motif protein family member 65 (TRIM65) belongs to the tripartite motif (TRIM) protein family. Its typical structure consists of the RING, B-Box motif, and coiled-coil domains, which are highly conserved at the N-terminus and the variable SPRY domain at the C-terminus. TRIM65 is an E3 ubiquitin ligase that participates in physiological and pathological processes through the ubiquitination pathway, including intracellular signal transduction, protein degradation, cell proliferation, apoptosis, carcinogenesis, autophagy, and phenotypic transformation. Evidence shows that TRIM65 plays a remarkable and obscure role in diseases, including multisystem tumours, neurodegenerative diseases, immune system diseases, and inflammatory diseases. This review is devoted to elaborating on the relationship between TRIM65 and diseases and its pathogenic mechanism, providing a theoretical basis for TRIM65 as a possible pathogenic target of diseases and exploring the possible future research direction of TRIM65 and the challenges it may face.
摘要：
Atherosclerosis is a chronic inflammatory disease of the arterial wall caused by an imbalance of lipid metabolism and a maladaptive inflammatory response. A variety of harmful cellular changes associated with atherosclerosis include endothelial dysfunction, the migration of circulating inflammatory cells to the arterial wall, the production of proinflammatory cytokines, lipid buildup in the intima, local inflammatory responses in blood vessels, atherosclerosis-associated apoptosis, and autophagy. PTEN inhibits the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/AKT)/mammalian target of rapamycin (mTOR) pathway through its lipid phosphatase activity. Previous studies have shown that PTEN is closely related to atherosclerosis. This article reviews the role of PTEN in atherosclerosis from the perspectives of autophagy, apoptosis, inflammation, proliferation, and angiogenesis.
