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Related Concept Videos

Disorders of the Skeletal Muscle01:28

Disorders of the Skeletal Muscle

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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
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Cross-bridge Cycle01:26

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As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
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Myocarditis I: Introduction01:21

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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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Proteins are broken down into amino acids during digestion. Unlike fats and carbohydrates, which are stored for later use, proteins are not. Instead, amino acids are either used to produce ATP through oxidation or contribute to the creation of new proteins for the growth and repair of the body. Any surplus amino acids from the diet are converted into glucose or triglycerides rather than excreted.
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Myasthenia Gravis: Overview and Treatment01:20

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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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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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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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Inflammation and Skeletal Muscle Wasting During Cachexia.

Justine M Webster1,2,3, Laura J A P Kempen1, Rowan S Hardy2,4,5

  • 1Department of Respiratory Medicine, NUTRIM School of Nutrition and Translational Research in Metabolism, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands.

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Inflammation drives cachexia, the loss of muscle and fat, impacting cancer and chronic disease patients. Understanding pro-inflammatory cytokines is key to developing targeted therapies for this debilitating condition.

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COPDatrophycachexiacancercytokinesinflammationmuscle wasting

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathophysiology

Background:

  • Cachexia involves involuntary muscle and adipose tissue loss, significantly impacting patient mortality and treatment outcomes in cancer and chronic inflammatory diseases.
  • Pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), are implicated in cachexia pathophysiology, with elevated levels observed in certain cancers and inflammatory conditions like COPD and RA.
  • Preclinical models strongly suggest a causal role for systemic inflammation in the development of cachexia.

Purpose of the Study:

  • To explore the mechanisms by which pro-inflammatory cytokines mediate muscle and fat wasting in cachexia.
  • To investigate the direct and indirect pathways through which inflammation affects skeletal muscle metabolism and body composition.
  • To highlight the potential of myokines as mediators and therapeutic targets in cachexia.

Main Methods:

  • Review of existing literature on pro-inflammatory cytokines, inflammation, and cachexia.
  • Analysis of association studies reporting cytokine levels in disease states.
  • Examination of preclinical animal models demonstrating the impact of inflammation on muscle and fat metabolism.
  • Investigation of molecular mechanisms including protein synthesis, catabolism (UPS, autophagy), myogenesis, and hormonal axes (HPA).

Main Results:

  • Pro-inflammatory cytokines directly inhibit muscle protein synthesis (MPS) and promote catabolism via the ubiquitin-proteasomal system (UPS) and autophagy.
  • Systemic inflammation indirectly contributes to muscle wasting by affecting the HPA axis, digestive system (anorexia-cachexia), liver, and adipocytes.
  • Myokines secreted by muscle act as autocrine and endocrine factors, modulating cachexia progression.

Conclusions:

  • Inflammation plays a pivotal role in cachexia development through complex direct and indirect mechanisms involving multiple signaling pathways.
  • Further research is needed to elucidate cytokine contributions to disease progression for biomarker discovery and targeted therapy development.
  • Identifying at-risk patients and developing interventions to prevent or delay cachexia progression are critical clinical goals.