Mechanistic insights of neuronal calcium and IP3 signaling system regulating ATP release during ischemia in progression of Alzheimer’s disease

IF 2.2 4区生物学 Q3 BIOPHYSICS

European Biophysics Journal Pub Date : 2023-05-24 DOI:10.1007/s00249-023-01660-1

Anand Pawar, Kamal Raj Pardasani

{"title":"Mechanistic insights of neuronal calcium and IP3 signaling system regulating ATP release during ischemia in progression of Alzheimer’s disease","authors":"Anand Pawar, Kamal Raj Pardasani","doi":"10.1007/s00249-023-01660-1","DOIUrl":null,"url":null,"abstract":"<div>The mechanisms of calcium ([Ca2+]) signaling in various human cells have been widely analyzed by scientists due to its crucial role in human organs like the heartbeat, muscle contractions, bone activity, brain functionality, etc. No study is reported for interdependent [Ca2+] and IP3 mechanics regulating the release of ATP in neuron cells during Ischemia in Alzheimer’s disease advancement. In the present investigation, a finite element method (FEM) is framed to explore the interdependence of spatiotemporal [Ca2+] and IP3 signaling mechanics and its role in ATP release during Ischemia as well as in the advancement of Alzheimer’s disorder in neuron cells. The results provide us insights of the mutual spatiotemporal impacts of [Ca2+] and IP3 mechanics as well as their contributions to ATP release during Ischemia in neuron cells. The results obtained for the mechanics of interdependent systems differ significantly from the results of simple independent system mechanics and provide new information about the processes of the two systems. From this study, it is concluded that neuronal disorders cannot only be simply attributed to the disturbance caused directly in the processes of calcium signaling mechanics, but also to the disturbances caused in IP3 regulation mechanisms impacting the calcium regulation in the neuron cell and ATP release.</div>","PeriodicalId":548,"journal":{"name":"European Biophysics Journal","volume":null,"pages":null},"PeriodicalIF":2.2000,"publicationDate":"2023-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Biophysics Journal","FirstCategoryId":"2","ListUrlMain":"https://link.springer.com/article/10.1007/s00249-023-01660-1","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOPHYSICS","Score":null,"Total":0}

引用次数: 3

Abstract

The mechanisms of calcium ([Ca²⁺]) signaling in various human cells have been widely analyzed by scientists due to its crucial role in human organs like the heartbeat, muscle contractions, bone activity, brain functionality, etc. No study is reported for interdependent [Ca²⁺] and IP₃ mechanics regulating the release of ATP in neuron cells during Ischemia in Alzheimer’s disease advancement. In the present investigation, a finite element method (FEM) is framed to explore the interdependence of spatiotemporal [Ca²⁺] and IP₃ signaling mechanics and its role in ATP release during Ischemia as well as in the advancement of Alzheimer’s disorder in neuron cells. The results provide us insights of the mutual spatiotemporal impacts of [Ca²⁺] and IP₃ mechanics as well as their contributions to ATP release during Ischemia in neuron cells. The results obtained for the mechanics of interdependent systems differ significantly from the results of simple independent system mechanics and provide new information about the processes of the two systems. From this study, it is concluded that neuronal disorders cannot only be simply attributed to the disturbance caused directly in the processes of calcium signaling mechanics, but also to the disturbances caused in IP₃ regulation mechanisms impacting the calcium regulation in the neuron cell and ATP release.

Abstract Image

查看原文本刊更多论文

神经元钙和IP3信号系统在阿尔茨海默病缺血过程中调节ATP释放的机制

由于钙([Ca2+])在人体器官如心跳、肌肉收缩、骨骼活动、大脑功能等中起着至关重要的作用，科学家们广泛分析了各种人体细胞中钙([Ca2+])信号传导的机制。在阿尔茨海默病进展过程中，神经元细胞在缺血过程中相互依赖的[Ca2+]和IP3机制调节ATP的释放尚未有研究报道。在本研究中，采用有限元法(FEM)探讨时空[Ca2+]和IP3信号机制的相互依赖性及其在缺血时ATP释放和阿尔茨海默病进展中的作用。这些结果为我们提供了[Ca2+]和IP3相互时空影响的机制，以及它们对神经元细胞缺血时ATP释放的贡献。相互依赖系统力学的结果与简单的独立系统力学的结果有很大的不同，并提供了关于这两个系统过程的新信息。本研究认为，神经元疾病不能简单地归结为钙信号传导机制过程中直接受到的干扰，还可以归结为IP3调节机制受到的干扰影响了神经元细胞内钙的调节和ATP的释放。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

European Biophysics Journal 生物-生物物理

CiteScore

4.30

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： The journal publishes papers in the field of biophysics, which is defined as the study of biological phenomena by using physical methods and concepts. Original papers, reviews and Biophysics letters are published. The primary goal of this journal is to advance the understanding of biological structure and function by application of the principles of physical science, and by presenting the work in a biophysical context. Papers employing a distinctively biophysical approach at all levels of biological organisation will be considered, as will both experimental and theoretical studies. The criteria for acceptance are scientific content, originality and relevance to biological systems of current interest and importance. Principal areas of interest include: - Structure and dynamics of biological macromolecules - Membrane biophysics and ion channels - Cell biophysics and organisation - Macromolecular assemblies - Biophysical methods and instrumentation - Advanced microscopics - System dynamics.