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Fatigue01:21

Fatigue

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Fatigue occurs when materials rupture under repeated or fluctuating loads, even at stress levels far below their static breaking strength. It typically results in brittle failure, even for ductile materials. It is a critical consideration in designing machines and structural components subjected to repetitive or varying loads. The nature of these loadings can range from fluctuating loads like unbalanced pump impellers causing vibrations to repeatedly bending a thin steel rod wire back and forth...
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Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective...
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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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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
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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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Myasthenia Gravis: Diagnostic Tests01:15

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Mitochondrial dysfunction and fatigue in Sjögren's disease.

Biji T Kurien1,2, John Aubrey Ice1,2, Rebecca A Wood2,3

  • 1Research, US Department of Veterans Affairs, Oklahoma City, Oklahoma, USA.

RMD Open
|April 24, 2025
PubMed
Summary

Mitochondrial dysfunction in T cells is linked to fatigue in Sjögren's disease (SjD). Impaired cellular energy production and altered mitophagy pathways contribute to SjD symptoms, highlighting a need for further research.

Keywords:
AutoimmunityFatigueInflammationSjogren's SyndromeT-Lymphocytes

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Area of Science:

  • Immunology
  • Cellular Biology
  • Metabolic Research

Background:

  • Sjögren's disease (SjD) is a chronic autoimmune disorder characterized by inflammation, dryness, and significant fatigue.
  • Fatigue in SjD may stem from impaired cellular bioenergetics, specifically mitochondrial dysfunction.
  • Mitochondria, the cell's powerhouses, are normally recycled via mitophagy; impaired mitophagy leads to the accumulation of dysfunctional mitochondria and increased oxidative stress.

Purpose of the Study:

  • To investigate the hypothesis that mitochondrial dysregulation in T cells is associated with fatigue in Sjögren's disease.
  • To explore the role of mitophagy in the pathogenesis of SjD-related fatigue.

Main Methods:

  • A case-control study involving T cells isolated from Sjögren's disease (SjD) patients, non-Sjögren's sicca (NSS) subjects, and healthy controls.
  • Analysis of T cell mitochondrial respiration using Seahorse technology (measuring oxygen consumption rate and extracellular acidification rate).
  • Bioinformatic analysis of public microarray data to identify a mitophagic transcriptional signature and stratify SjD patients.

Main Results:

  • T cells from SjD and NSS subjects exhibited significantly lower basal oxygen consumption rate (OCR), ATP-linked respiration, maximal respiration, and reserve capacity compared to healthy individuals.
  • No significant differences were observed in non-mitochondrial respiration, basal glycolysis, or glycolytic reserve between groups.
  • Fatigue measures correlated with altered OCR in SjD patients, and transcriptional analysis revealed dynamic changes related to mitophagy pathways.

Conclusions:

  • Mitochondrial dysfunction is a significant feature in Sjögren's disease T cells.
  • Impaired mitochondrial function and altered mitophagy pathways are strongly associated with fatigue in SjD.
  • These findings underscore the importance of investigating mitochondrial health and bioenergetics in SjD management.