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Related Concept Videos

Mitochondrial Membranes01:45

Mitochondrial Membranes

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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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Mitochondria01:37

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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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Updated: Oct 21, 2025

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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Mitochondrial dysfunction in perinatal asphyxia: role in pathogenesis and potential therapeutic interventions.

Puneet K Samaiya1, Sairam Krishnamurthy2, Ashok Kumar3

  • 1Department of Pharmacy, Shri G.S. Institute of Technology and Science, Indore, MP, 452003, India. punit.samaiya@gmail.com.

Molecular and Cellular Biochemistry
|September 2, 2021
PubMed
Summary

Perinatal asphyxia causes brain injury through complex cell death pathways. Targeting mitochondrial dysfunction offers promising new therapies, alone or with therapeutic hypothermia, for newborns.

Keywords:
ApoptosisApoptosomeExcitotoxicityHypoxic-ischemic encephalopathyMitochondriaPerinatal asphyxia

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The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
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The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Neonatal Medicine

Background:

  • Perinatal asphyxia (PA) can lead to hypoxic-ischemic encephalopathy and long-term neurological deficits in newborns.
  • Brain injury post-PA involves a transition from necrosis to apoptosis, driven by excitotoxicity, oxidative stress, and mitochondrial dysfunction.
  • Current treatment, therapeutic hypothermia, improves outcomes but new interventions are needed.

Purpose of the Study:

  • To explore mitochondrial pathways involved in perinatal asphyxia brain injury.
  • To review current and past therapeutic strategies targeting these pathways.
  • To identify novel therapeutic interventions for neonatal brain injury.

Main Methods:

  • Review of scientific literature on perinatal asphyxia and neonatal brain injury.
  • Analysis of pathomechanisms including excitotoxicity, oxidative stress, and mitochondrial dysfunction.
  • Evaluation of therapeutic hypothermia and potential mitoprotective therapies.

Main Results:

  • Mitochondrial dysfunction, including suppressed respiration and calcium dysregulation, is central to PA-induced neuronal death.
  • Bax-dependent mitochondrial permeabilization, cytochrome c release, and caspase activation drive cell death.
  • Therapeutic hypothermia is effective but mitoprotective therapies present a promising complementary approach.

Conclusions:

  • Mitochondrial pathways are critical targets for treating perinatal asphyxia brain injury.
  • Mitoprotective therapies, potentially combined with therapeutic hypothermia, offer new hope for affected newborns.
  • Further research into targeting these pathways is essential for developing novel interventions.