通过LPEAT-mitophagy通路,TMAO促进血管内皮细胞的灭
Yanmei Chen1, Chuchu Yuan2, Wenhua Qin2
1Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China; Department of Pathology, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Biochemical and biophysical research communications
|February 21, 2024
概括
三甲基胺N-氧化物 (TMAO) 通过在内皮细胞中引起过度的髓和热,促进动脉样硬化. 这一过程与酸丁乙醇胺酸转移酶 (LPEAT) 的上调有关,这表明LPEAT是潜在的治疗点.
科学领域:
- 心血管科学 心血管科学
- 细胞生物学 细胞生物学
- 分子医学是分子医学.
背景情况:
- 三甲基胺N氧化物 (TMAO) 是动脉样硬化的新兴危险因素.
- 炎症驱动的血管内皮损伤是动脉动脉生成的核心.
- 炎症性编程细胞死亡的热,加剧了动脉样硬化.
研究的目的:
- 研究TMAO诱导血管内皮细胞损伤的机制.
- 探索菌体和热在TMAO介导的动脉动脉生成中的作用.
- 为了确定潜在的分子点,以减轻TMAO的影响.
主要方法:
- 用TMAO治疗了内皮细胞培养.
- 用特定的标记物评估了线粒的水平.
- 通过caspase-1活性和IL-1β释放量度Pyroptosis.
- 分析了酸丁乙醇胺酸转移酶 (LPEAT) 的表达.
主要成果:
- 治疗TMAO导致内皮细胞中过度的线粒.
- 这种过度的线粒会促进热.
- TMAO上调调节了LPEAT的表达,调解了观察到的效应.
- 在TMAO诱导的内皮细胞损伤中,LPEAT似乎是关键的调解者.
结论:
- TMAO诱导内皮细胞损伤,并通过过度的线粒和热死促进动脉样硬化.
- LPEAT在调解TMAO诱导的热中起着至关重要的作用.
- 针对LPEAT可能为动脉样硬化预防和治疗提供一种新的治疗策略.
相关概念视频
The Extrinsic Apoptotic Pathway
6.4K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.4K
Overview of Cell Death
7.3K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
7.3K
Autophagic Cell Death
3.4K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.4K
The Intrinsic Apoptotic Pathway
6.5K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.5K
PI3K/mTOR/AKT Signaling Pathway
3.6K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.6K
Phagocytosis of Apoptotic Cells
3.8K
Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized...
Normal cells contain receptors that prevent them from being recognized...
3.8K


