METTL3通过调节铁灭菌来控制胸细胞的发育和胸膜内变
Huiru Jing1,2, Jiayu Song1,2, Jie Sun1,2
1Department of Urology, State Key Laboratory of Virology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Nature aging
|October 24, 2024
概括
研究人员发现,蛋白质METTL3 (甲基转移酶样蛋白3) 阻止了胸细胞中的铁,这是免疫衰老的关键过程. 恢复METTL3功能可能有助于逆转胸膜内置并恢复免疫功能.
科学领域:
- 免疫学 免疫学 免疫学
- 衰老研究研究 衰老研究
- 细胞生物学 细胞生物学
背景情况:
- 胸膜内置,免疫衰老的标志,涉及复杂的细胞过程.
- 细胞死亡途径,特别是铁亡,在胸膜内变的精确作用仍然在很大程度上是未知的.
- 识别胸膜内变的调节者对于理解和潜在地减轻免疫衰退至关重要.
研究的目的:
- 为了研究甲基转移酶样蛋白3 (METTL3) 在胸膜卷发中的作用.
- 阐明METTL3影响小细胞存活和衰老的机制.
- 探索针对铁质的治疗策略,以恢复胸膜功能.
主要方法:
- 在老年小鼠中分析CD4+CD8+双阳性 (DP) 胸细胞.
- 在T细胞中条件删除METTL3.
- 评估铁灭症信号和谷氨过氧化酶4 (GPX4) 水平.
- 药理上抑制铁灭的作用.
主要成果:
- 年龄较大的DP胸细胞表现出衰老和减少METTL3表达.
- 在T细胞中METTL3缺乏会加剧DP小胞老化,并促进铁亡.
- 在转化层面上,METTL3维持GPX4,独立于其甲基转移酶活性.
- 抑制铁灭可以挽救DP细胞的存活率,并减轻衰老特征.
结论:
- METTL3在预防铁亡和抑制胸膜内变方面发挥着至关重要的作用.
- METTL3调节GPX4的翻译,从而控制DP胸细胞中的铁亡.
- 准METTL3调节的铁亡是一种潜在的策略,可以恢复老年人的胸膜功能.
相关概念视频
Necrosis
4.4K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.4K
Receptor Downregulation in MVBs
2.0K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
2.0K
Regulation of Hematopoietic Stem Cells
3.1K
All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
3.1K
TGF - β Signaling Pathway
7.2K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.2K


