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内皮细胞的衰老促进了进发性纤维细胞的表型变化:对血管衰老的可能影响

Katarzyna Sarad^1,2, Urszula Jankowska³, Bozena Skupien-Rabian³

¹Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa Str. 7, 30-387, Krakow, Poland.

Molecular and cellular biochemistry

|May 14, 2024

概括

血管中的细胞衰老会释放GDF-15等因素,影响纤维细胞功能,并可能导致血管疾病. 向衰老或铁亡可能会提供新的治疗途径.

科学领域:

心血管生物学心血管生物学
细胞衰老细胞衰老
分子医学是分子医学.

背景情况:

老龄化是心血管疾病的主要危险因素.
衰老细胞分泌出改变血管壁功能的因素 (衰老相关的分泌表型).
内皮细胞衰老对进发性的影响尚不清楚.

研究的目的:

为了描述氧化应激诱导的内皮细胞衰老.
为了确定老化的内皮细胞对偶然性纤维细胞的膜效应.
调查增长差异化因素15 (GDF-15) 在这些相互作用中的作用.

主要方法:

人类大动脉内皮细胞 (HAEC) 使用过氧化诱导过早衰老.
蛋白质组分析 (质谱) 在老化HAEC和用条件介质处理的纤维细胞上进行.
用重组GDF-15和基因沉默来研究其特定效应.

主要成果:

衰老的HAEC显示出高调节的GDF-15分泌.
从衰老HAEC的条件介质改变了纤维细胞蛋白质,影响了脂蛋白代谢,线粒和铁亡.
GDF-15影响了一些铁灭菌标记物,并减少了纤维细胞中的氧化应激,但沉默GDF-15保护了铁灭菌.

结论:

内皮细胞衰老影响进发性纤维细胞,部分通过GDF-15.
纤维细胞中与衰老相关的变化涉及脂蛋白代谢和细胞死亡途径,如铁亡.
针对细胞衰老和铁亡的治疗策略可能对血管疾病有益.

关键词:

进入性纤维细胞.内皮细胞衰老细胞衰老铁化是铁化的一种.这是GDF-15的GDF-15.氧化应激是一种氧化应激.

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