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Corrigendum to “SEMA4D acts as a novel oligogenic pathogenic gene of idiopathic hypogonadotropic hypogonadism through the PlexinB1/MET/RND1/RHOA/RAF1/MAPK signaling axis” [Genes & Diseases 10 (2023) 65–68] 对 "SEMA4D通过PlexinB1/MET/RND1/RHOA/RAF1/MAPK信号轴作为特发性性腺功能减退症的新型寡致病基因 "的更正 [Genes & Diseases 10 (2023) 65-68]
IF 6.8 2区 医学 Q1 Medicine Pub Date : 2024-03-22 DOI: 10.1016/j.gendis.2024.101273
Daoqi Wang , Yonghua Niu , Jiahong Tan , Jiaxin Wang , Le Ling , Yinwei Chen , Jianan Gong , Hao Xu , Qing Ling , Jianhe Liu , Jihong Liu
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引用次数: 0
The link between ten-eleven translocation-2 (Tet2) related clonal hematopoiesis and sequential onset of two hematologic malignancies 十-十一易位-2(Tet2)相关克隆造血与两种血液恶性肿瘤相继发病之间的联系
IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-03-22 DOI: 10.1016/j.gendis.2024.101270
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引用次数: 0
VPS13D affects epileptic seizures by regulating mitochondrial fission and autophagy in epileptic rats VPS13D 通过调节线粒体分裂和自噬影响癫痫大鼠的癫痫发作
IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-03-19 DOI: 10.1016/j.gendis.2024.101266

Abnormal mitochondrial dynamics can lead to seizures, and improved mitochondrial dynamics can alleviate seizures. Vacuolar protein sorting 13D (VPS13D) is closely associated with regulating mitochondrial homeostasis and autophagy. However, further investigation is required to determine whether VPS13D affects seizures by influencing mitochondrial dynamics and autophagy. We aimed to investigate the influence of VPS13D on behavior in a rat model of acute epileptic seizures. Hence, we established an acute epileptic seizure rat model and employed the CRISPR/CAS9 technology to construct a lentivirus to silence the Vps13d gene. Furthermore, we used the HT22 mouse hippocampal neuron cell line to establish a stable strain with suppressed expression of Vps13d in vitro. Then, we performed quantitative proteomic and bioinformatics analyses to confirm the mechanism by which VPS13D influences mitochondrial dynamics and autophagy, both in vitro and in vivo using the experimental acute epileptic seizure model. We found that knockdown of Vps13d resulted in reduced seizure latency and increased seizure frequency in the experimental rats. Immunofluorescence staining and western blot analysis revealed a significant increase in mitochondrial dynamin-related protein 1 expression following Vps13d knockdown. Moreover, we observed a significant reduction in LC3II protein expression levels and the LC3II/LC3I ratio (indicators for autophagy) accompanied by a significant increase in P62 expression (an autophagy adaptor protein). The proteomic analysis confirmed the up-regulation of P62 protein expression. Therefore, we propose that VPS13D plays a role in modulating seizures by influencing mitochondrial dynamics and autophagy.

线粒体动力学异常可导致癫痫发作,而改善线粒体动力学可减轻癫痫发作。空泡蛋白分选 13D(VPS13D)与调节线粒体平衡和自噬密切相关。然而,要确定VPS13D是否会通过影响线粒体动力学和自噬来影响癫痫发作,还需要进一步的研究。我们旨在研究 VPS13D 对急性癫痫发作大鼠模型行为的影响。因此,我们建立了一个急性癫痫发作大鼠模型,并采用 CRISPR/CAS9 技术构建了一种慢病毒来沉默 Vps13d 基因。此外,我们还利用 HT22 小鼠海马神经元细胞系建立了体外抑制 Vps13d 表达的稳定株系。然后,我们进行了定量蛋白质组学和生物信息学分析,利用实验性急性癫痫发作模型证实了 VPS13D 在体外和体内影响线粒体动力学和自噬的机制。我们发现,敲除 Vps13d 会导致实验鼠癫痫发作潜伏期缩短、发作频率增加。免疫荧光染色和 Western 印迹分析表明,敲除 Vps13d 后线粒体动态相关蛋白 1 的表达显著增加。此外,我们还观察到 LC3II 蛋白表达水平和 LC3II/LC3I 比值(自噬指标)显著降低,同时 P62(自噬适配蛋白)表达显著增加。蛋白质组分析证实了 P62 蛋白表达的上调。因此,我们认为 VPS13D 通过影响线粒体动力学和自噬在调节癫痫发作中发挥作用。
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引用次数: 0
Integrating single-cell RNA sequencing and bulk RNA sequencing data to predict acute respiratory distress syndrome in sepsis patients 整合单细胞 RNA 测序和大量 RNA 测序数据,预测脓毒症患者的急性呼吸窘迫综合征
IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-03-19 DOI: 10.1016/j.gendis.2024.101271
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引用次数: 0
Identification of AAV serotypes for gene therapy in Krabbe iPSCs-derived brain organoids 鉴定用于克雷伯iPSCs衍生脑器官组织基因治疗的AAV血清型
IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-03-19 DOI: 10.1016/j.gendis.2024.101269
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引用次数: 0
The combination of SLC7A11 inhibitor and oridonin synergistically inhibits cervical cancer cell growth by decreasing the NADPH/NADP+ ratio SLC7A11 抑制剂与奥利多宁的组合通过降低 NADPH/NADP+ 比率协同抑制宫颈癌细胞的生长
IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-03-19 DOI: 10.1016/j.gendis.2024.101265
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引用次数: 0
NUF2 overexpression predicts poor outcomes in multiple myeloma NUF2过表达可预测多发性骨髓瘤的不良预后
IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-03-19 DOI: 10.1016/j.gendis.2024.101268
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引用次数: 0
Mechanosensitive adhesion G protein-coupled receptors: Insights from health and disease 机械敏感粘附 G 蛋白偶联受体:健康与疾病的启示
IF 6.8 2区 医学 Q1 Medicine Pub Date : 2024-03-16 DOI: 10.1016/j.gendis.2024.101267
Shiying Sun, Wen Wang
Ontogeny cannot be separated from mechanical forces. Cells are continuously subjected to different types of mechanical stimuli that convert into intracellular signals through mechanotransduction. As a member of the G protein-coupled receptor superfamily, adhesion G protein-coupled receptors (aGPCRs) have attracted extensive attention due to their unique extracellular domain and adhesion properties. In the past few decades, increasing evidence has indicated that sensing mechanical stimuli may be one of the main physiological activities of aGPCRs. Here, we review the general structure and activation mechanisms of these receptors and highlight the lesion manifestations relevant to each mechanosensitive aGPCR.
本体发育离不开机械力。细胞不断受到不同类型的机械刺激,这些刺激通过机械传导转化为细胞内信号。作为 G 蛋白偶联受体超家族的一员,粘附 G 蛋白偶联受体(aGPCR)因其独特的胞外结构域和粘附特性而受到广泛关注。过去几十年来,越来越多的证据表明,感知机械刺激可能是 aGPCR 的主要生理活动之一。在此,我们回顾了这些受体的一般结构和激活机制,并重点介绍了与每种机械敏感性 aGPCR 相关的病变表现。
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引用次数: 0
Focus on cardiac troponin complex: From gene expression to cardiomyopathy 聚焦心肌肌钙蛋白复合物:从基因表达到心肌病
IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-03-11 DOI: 10.1016/j.gendis.2024.101263

The cardiac troponin complex (cTn) is a regulatory component of sarcomere. cTn consists of three subunits: cardiac troponin C (cTnC), which confers Ca2+ sensitivity to muscle; cTnI, which inhibits the interaction of cross-bridge of myosin with thin filament during diastole; and cTnT, which has multiple roles in sarcomere, such as promoting the link between the cTnI-cTnC complex and tropomyosin within the thin filament and influencing Ca2+ sensitivity of cTn and force development during contraction. Conditions that interfere with interactions within cTn and/or other thin filament proteins can be key factors in the regulation of cardiac contraction. These conditions include alterations in myofilament Ca2+ sensitivity, direct changes in cTn function, and triggering downstream events that lead to adverse cardiac remodeling and impairment of heart function. This review describes gene expression and post-translational modifications of cTn as well as the conditions that can adversely affect the delicate balance among the components of cTn, thereby promoting contractile dysfunction.

心肌肌钙蛋白复合物(cTn)是肌节的调节成分。cTn 由三个亚基组成:心肌肌钙蛋白 C(cTnC),它赋予肌肉对钙的敏感性;cTnI,它在舒张过程中抑制肌球蛋白与细丝的交桥相互作用;cTnT,它在肌浆中具有多种作用,如促进 cTnI-cTnC 复合物与细丝内肌球蛋白之间的联系,影响 cTn 对钙的敏感性和收缩过程中的力量发展。干扰 cTn 和/或其他细丝蛋白内部相互作用的条件可能是调节心脏收缩的关键因素。这些情况包括改变肌丝对 Ca 的敏感性、直接改变 cTn 功能以及引发下游事件,从而导致不良的心脏重塑和心脏功能损害。本综述介绍了 cTn 的基因表达和翻译后修饰,以及可能对 cTn 各成分之间的微妙平衡产生不利影响从而导致收缩功能障碍的情况。
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引用次数: 0
Pdgfrα+ stromal cells, a key regulator for tissue homeostasis and dysfunction in distinct organs Pdgfrα+基质细胞--不同器官组织稳态和功能障碍的关键调节因子
IF 6.8 2区 医学 Q1 Medicine Pub Date : 2024-03-09 DOI: 10.1016/j.gendis.2024.101264
Xia Kang, Kun Zhao, Zhu Huang, So-ichiro Fukada, Xiao-wei Qi, Hongming Miao
Pdgfrα stromal cells are a group of cells specifically expressing Pdgfrα, which may be mentioned with distinct names in different tissues. Importantly, the findings from numerous studies suggest that these cells share exactly similar biomarkers and properties, show complex functions in regulating the microenvironment, and are critical to tissue regeneration, repair, and degeneration. Comparing the similarities and differences between distinct tissue-resident Pdgfrα stromal cells is helpful for us to more comprehensively and deeply understand the behaviors of these cells and to explore some common regulating mechanisms and therapeutical targets. In this review, we summarize previous and current findings on Pdgfrα stromal cells in various tissues and discuss the crosstalk between Pdgfrα stromal cells and microenvironment.
Pdgfrα 基质细胞是一组特异性表达 Pdgfrα 的细胞,在不同的组织中可能有不同的名称。重要的是,大量研究结果表明,这些细胞具有完全相似的生物标志物和特性,在调节微环境方面显示出复杂的功能,对组织再生、修复和退化至关重要。比较不同组织驻留的Pdgfrα基质细胞之间的异同有助于我们更全面、深入地了解这些细胞的行为,并探索一些共同的调控机制和治疗靶点。在这篇综述中,我们总结了以前和现在关于不同组织中Pdgfrα基质细胞的研究结果,并讨论了Pdgfrα基质细胞与微环境之间的相互影响。
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引用次数: 0
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