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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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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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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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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.
ROS generation is regulated and maintained at moderate levels necessary...
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Translocation of Proteins into the Mitochondria01:19

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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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 and therapeutic perspectives in osteoporosis.

Jialing Liu1, Zhonghua Gao2, Xiangjie Liu1

  • 1Department of Geriatrics, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Frontiers in Endocrinology
|February 19, 2024
PubMed
Summary

Mitochondrial dysfunction, marked by altered DNA, impaired energy production, and increased oxidative stress, significantly contributes to osteoporosis. Targeting mitochondria offers promising therapeutic avenues for this bone disease.

Keywords:
mitochondrial dysfunctionmitochondrial quality controlosteoporosisoxidative phosphorylationreactive oxygen species

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Orthopedics

Background:

  • Osteoporosis (OP) is a skeletal disorder characterized by low bone mass and tissue deterioration, increasing fracture risk.
  • An imbalance in bone resorption and formation processes underlies OP pathogenesis.
  • Mitochondrial dysfunction is increasingly recognized as a key factor in OP development.

Purpose of the Study:

  • To review the correlation between various aspects of mitochondrial dysfunction and osteoporosis.
  • To explore potential therapeutic strategies targeting mitochondria for osteoporosis treatment.

Main Methods:

  • Literature review and analysis of studies investigating mitochondrial dysfunction in osteoporosis.
  • Examination of mitochondrial DNA alterations, oxidative phosphorylation (OXPHOS) impairment, mitophagy, biogenesis, dynamics, and reactive oxygen species (ROS) accumulation in OP.

Main Results:

  • Mitochondrial dysfunction, including mtDNA alterations, OXPHOS impairment, and excessive ROS, is closely linked to osteoporosis.
  • Dysfunctional mitochondria disrupt the balance between bone formation and resorption, exacerbating bone fragility.

Conclusions:

  • Mitochondrial dysfunction is a critical mechanism in osteoporosis pathogenesis.
  • Modulating mitochondrial function presents a promising therapeutic strategy for osteoporosis, although further research is needed for clinical application.