Molecular mechanisms of the mitochondrial permeability transition

线粒体通透性转变的分子机制

基本信息

  • 批准号:
    10322360
  • 负责人:
  • 金额:
    $ 43.11万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2021
  • 资助国家:
    美国
  • 起止时间:
    2021-02-01 至 2026-01-31
  • 项目状态:
    未结题

项目摘要

The overarching goal of my research program is to identify and characterize molecular mechanisms responsible for stress-induced permeabilization of the mitochondrial inner membrane. In most eukaryotic cells, mitochondria are the primary source of the energy that they provide in the form of ATP by performing oxidative phosphorylation (OXPHOS). OXPHOS is a two-step process. First, substrate oxidation by the respiratory chain results in the generation of the electrical potential on the mitochondrial inner membrane. This potential energy drives generation of ATP by the phosphorylation of ADP at the ATP synthase complex. To prevent energy dissipation and ensure that OXPHOS is efficient mitochondrial inner membrane permeability should be tightly controlled and maintained at low levels. Stress conditions associated with dysregulation of calcium and ROS homeostasis can lead to an increase in mitochondrial inner membrane permeability – a phenomenon known as Mitochondrial Permeability Transition (mPT). mPT causes dissipation of the membrane potential and loss of mitochondrial ATP-generating capacity leading to cell dysfunction and death. mPT is critically involved in a broad spectrum of diseases ranging from heart attack to neurodegeneration. Prevention of mPT is highly protective against cell death and tissue damage suggesting high therapeutics potential. However, molecular mechanisms of mPT are not well understood, and this gap in knowledge prevents mPT from being a drug target. Over the past five years, we demonstrated that mPT is a multifaceted phenomenon and depending on the disease type and stress severity, it can occur through different pathways. The central goal of our research program is to identify the link between specific molecular mechanisms of mPT and specific stress conditions. We have already established several original animal and cell disease-relevant models causing different types of mPT. In our approach, a variety of methods that measure the mPT and tissue damage at the organismal, cellular and mitochondrial levels are coupled with a number of our original electrophysiological (patch- clamp) assays that allow direct measurement of mPT at the level of mitochondrial membranes and give us a unique opportunity to dissect and characterize its multiple identities and regulation. The results of our study will provide a detailed understanding of one of the most critical events in cell death cascades and will bring an essential framework for the development of therapeutically approaches that will selectively target mPT.
我的研究计划的首要目标是识别和表征分子机制

项目成果

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Evgeny Pavlov其他文献

Evgeny Pavlov的其他文献

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{{ truncateString('Evgeny Pavlov', 18)}}的其他基金

Molecular mechanisms of the mitochondrial permeability transition
线粒体通透性转变的分子机制
  • 批准号:
    10557809
  • 财政年份:
    2021
  • 资助金额:
    $ 43.11万
  • 项目类别:
Molecular mechanisms of the mitochondrial permeability transition
线粒体通透性转变的分子机制
  • 批准号:
    10728363
  • 财政年份:
    2021
  • 资助金额:
    $ 43.11万
  • 项目类别:
Molecular mechanisms of the mitochondrial permeability transition
线粒体通透性转变的分子机制
  • 批准号:
    10551711
  • 财政年份:
    2021
  • 资助金额:
    $ 43.11万
  • 项目类别:
Molecular composition of the mitochondrial permeability transition pore
线粒体通透性转换孔的分子组成
  • 批准号:
    10004077
  • 财政年份:
    2016
  • 资助金额:
    $ 43.11万
  • 项目类别:

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