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Stefan Günther

max-planck-institute for heart and lung research
H指数:44
被引数:7,565

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Hematopoietic loss of KDM6A impairs cardiac recovery in heart failure via epigenetic reprogramming of myeloid cells

造血系统KDM6A缺失通过髓系细胞的表观遗传重编程损害心力衰竭的心脏恢复

2026-11-030
OA
Endothelial soluble APP/APLP2 promote heart repair through KIT-mediated angiogenesis

内皮细胞可溶性APP/APLP2通过KIT介导的血管生成促进心脏修复

2026-05-220
OA
Soluble epoxide hydrolase drives neurovascular dysfunction in a model of amyloidosis

可溶性环氧水解酶驱动淀粉样变性模型中的神经血管功能障碍

Brain
IF11.7
2026-05-220
PRE
Identification of unannotated microproteins involved in endothelial cell homeostasis, dysfunction and vascular disease

鉴定参与内皮细胞稳态、功能障碍和血管疾病的未注释微小蛋白

2026-05-190
OAAI
TNF superfamily member 14 drives post-influenza depletion of alveolar macrophages, enabling secondary pneumococcal pneumonia

肿瘤坏死因子超家族成员14驱动流感后肺泡巨噬细胞耗竭,促进继发性肺炎链球菌肺炎

2026-01-160
OA
Atherosclerosis licenses for an exceeding immune response in COVID-19 disease by interferon priming in circulating myeloid cells

动脉粥样硬化通过循环髓系细胞中的干扰素预激活,引发COVID-19疾病中过度的免疫反应

2026-01-011
PRE
Transcription regulation by TBX18 in smooth muscle cells is essential for normal aortic development and homeostasis

TBX18在平滑肌细胞中对转录的调控对于正常主动脉发育和稳态维持至关重要。

2025-11-011
PRE
Cystine import and oxidative catabolism fuel vascular growth and repair via nutrient-responsive histone acetylation

胱氨酸的摄取和氧化分解通过营养响应性组蛋白乙酰化促进血管生长和修复。

2025-10-310
OAAI
Orphan receptor GPR153 facilitates vascular damage responses by modulating cAMP levels, YAP/TAZ signaling, and NF-κB activation

孤儿受体GPR153通过调节cAMP水平、YAP/TAZ信号通路和NF-κB活化来促进血管损伤反应。

2025-07-070
OAAI
Transcriptional changes of the extracellular matrix in chronic thromboembolic pulmonary hypertension govern right ventricle remodeling and recovery

细胞外基质转录变化在慢性血栓栓塞性肺动脉高压中调控右心室重塑与恢复

2025-07-040
OAAI
Orphan G protein-coupled receptor GPRC5B controls macrophage function by facilitating prostaglandin E receptor 2 signaling

孤儿G蛋白偶联受体GPRC5B通过促进前列腺素E受体2信号传导来调控巨噬细胞功能。

2025-02-070
OA