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Related Concept Videos

Mitochondria01:37

Mitochondria

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Electron Transport Chain: Complex I and II01:46

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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The Inner Mitochondrial Membrane01:28

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The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
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Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells
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High-density lipoprotein, mitochondrial dysfunction and cell survival mechanisms.

C Roger White1, Samantha Giordano1, G M Anantharamaiah2

  • 1Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA.

Chemistry and Physics of Lipids
|May 7, 2016
PubMed
Summary

High-density lipoprotein (HDL) components, apolipoprotein A-I and sphingosine 1-phosphate, protect the heart from ischemia/reperfusion injury by activating survival pathways and preventing mitochondrial damage.

Keywords:
ApoA-IHdlIschemia-reperfusionMitochondrionMyocardiumSphingosine 1-Phosphate

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Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Cellular Signaling

Background:

  • Ischemia/reperfusion (I/R) injury is a major complication following cardiac events and procedures.
  • Mitochondrial dysfunction, driven by reactive oxygen species (ROS) and opening of the mitochondrial permeability transition pore (mPTP), is central to I/R injury.
  • Ischemic conditioning protocols (preconditioning and postconditioning) protect the heart by activating RISK and SAFE pathways.

Purpose of the Study:

  • To review the role of high-density lipoprotein (HDL) and its components in mitigating myocardial I/R injury.
  • To elucidate the mechanisms by which HDL-associated mediators activate cardioprotective signaling cascades.
  • To highlight apolipoprotein A-I (apoA-I) and sphingosine 1-phosphate (S1P) as key players in HDL-mediated cardioprotection.

Main Methods:

  • Review of clinical and experimental studies on I/R injury and cardioprotective strategies.
  • Analysis of signaling pathways involved in cell survival, including RISK and SAFE pathways.
  • Investigation of the molecular targets of HDL components, such as ROS production and mPTP opening.

Main Results:

  • HDL mimics the protective effects of ischemic conditioning against myocardial I/R injury.
  • HDL activates the Reperfusion Injury Salvage Kinase (RISK) and Survivor Activating Factor Enhancement (SAFE) pathways.
  • Apolipoprotein A-I (apoA-I) and sphingosine 1-phosphate (S1P) mediate infarct-sparing effects by inhibiting ROS-dependent damage and mPTP opening.

Conclusions:

  • HDL, through apoA-I and S1P, represents a promising therapeutic strategy for attenuating myocardial I/R injury.
  • Targeting HDL-mediated signaling offers a novel approach to enhance cardiomyocyte survival and preserve cardiac function post-ischemia.
  • Understanding the interplay between HDL, mitochondria, and cell survival pathways is crucial for developing effective treatments for ischemic heart disease.