Suppr超能文献

体外线粒体肿胀的计算建模:一种生物物理方法。

Computational Modeling of In Vitro Swelling of Mitochondria: A Biophysical Approach.

机构信息

Department of Physics, University of Puerto Rico, Rio Piedras Campus, San Juan, PR 00931-3343, USA.

Faculty of Sciences and Technology, Department of Chemistry and Pharmacy, and Interdisciplinary Centre of Chemistry of Algarve, University of Algarve, 8005-139 Faro, Portugal.

出版信息

Molecules. 2018 Mar 28;23(4):783. doi: 10.3390/molecules23040783.

Abstract

Swelling of mitochondria plays an important role in the pathogenesis of human diseases by stimulating mitochondria-mediated cell death through apoptosis, necrosis, and autophagy. Changes in the permeability of the inner mitochondrial membrane (IMM) of ions and other substances induce an increase in the colloid osmotic pressure, leading to matrix swelling. Modeling of mitochondrial swelling is important for simulation and prediction of in vivo events in the cell during oxidative and energy stress. In the present study, we developed a computational model that describes the mechanism of mitochondrial swelling based on osmosis, the rigidity of the IMM, and dynamics of ionic/neutral species. The model describes a new biophysical approach to swelling dynamics, where osmotic pressure created in the matrix is compensated for by the rigidity of the IMM, i.e., osmotic pressure induces membrane deformation, which compensates for the osmotic pressure effect. Thus, the effect is linear and reversible at small membrane deformations, allowing the membrane to restore its normal form. On the other hand, the membrane rigidity drops to zero at large deformations, and the swelling becomes irreversible. As a result, an increased number of dysfunctional mitochondria can activate mitophagy and initiate cell death. Numerical modeling analysis produced results that reasonably describe the experimental data reported earlier.

摘要

线粒体肿胀通过凋亡、坏死和自噬刺激线粒体介导的细胞死亡,在人类疾病的发病机制中起着重要作用。离子和其他物质的线粒体内膜 (IMM) 通透性的变化导致胶体渗透压增加,从而导致基质肿胀。线粒体肿胀的建模对于模拟和预测细胞在氧化和能量应激期间体内事件非常重要。在本研究中,我们开发了一种计算模型,该模型基于渗透、IMM 的刚性和离子/中性物质的动力学来描述线粒体肿胀的机制。该模型描述了一种新的肿胀动力学的生物物理方法,其中基质中产生的渗透压由 IMM 的刚性来补偿,即渗透压诱导膜变形,从而补偿渗透压的影响。因此,在小的膜变形下,效果是线性和可逆的,允许膜恢复正常形态。另一方面,当膜变形较大时,膜刚性降至零,肿胀变得不可逆。结果,大量功能失调的线粒体可以激活细胞自噬并引发细胞死亡。数值建模分析产生的结果合理地描述了之前报道的实验数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb1b/6017623/5792dddf2426/molecules-23-00783-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验