Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

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.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Myasthenia Gravis: Diagnostic Tests01:15

Myasthenia Gravis: Diagnostic Tests

Myasthenia gravis is an autoimmune condition affecting neuromuscular transmission, causing generalized weakness in skeletal muscles. Initial diagnoses rely on patients' signs, symptoms, and medical history. The challenge lies in distinguishing myasthenia from other muscular dystrophies. An important diagnostic feature is the significant improvement of symptoms after administering anticholinesterase inhibitors.
The edrophonium test is a diagnostic tool for myasthenia gravis. It involves...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Strategic Amyotrophic Lateral Sclerosis Australia-Systems Genomics Consortium (SALSA-SGC): cohort profile.

BMJ open·2026
Same author

Characterising manual dexterity, motor cortex neuroplasticity, and intracortical inhibition long after burn injury.

Burns : journal of the International Society for Burn Injuries·2026
Same author

Evaluating ChatGPT's advice and recommendations regarding exercise for people with inclusion body myositis.

Neuromuscular disorders : NMD·2026
Same author

Plasma exchange in adult idiopathic inflammatory myositis: a systematic review and meta-analysis.

Clinical rheumatology·2026
Same author

Changes in body composition and phase angle from diagnosis to gastrostomy, in motor neuron disease patients: a longitudinal study.

European journal of clinical nutrition·2026
Same author

Large-scale drug screening in iPSC-derived motor neurons from sporadic ALS patients identifies a potential combinatorial therapy.

Nature neuroscience·2025
Same journal

New approaches to the management of cutaneous lupus.

Current opinion in rheumatology·2026
Same journal

"Updates in chronic nonbacterial osteomyelitis: emerging insights across the age spectrum".

Current opinion in rheumatology·2026
Same journal

Difficult-to-treat, complex-to-manage, treatment-refractory spondyloarthritis: semantics or substance?

Current opinion in rheumatology·2026
Same journal

Update on IgA nephropathy: implications for treatment in IgA vasculitis: a guide for rheumatologists.

Current opinion in rheumatology·2026
Same journal

Polyarticular juvenile idiopathic arthritis: insights from genetic studies on disease risk and pathogenesis.

Current opinion in rheumatology·2026
Same journal

Immune dysregulation in children with Down syndrome: clinical implications and emerging therapies.

Current opinion in rheumatology·2026
See all related articles

Related Experiment Video

Updated: May 29, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Published on: August 21, 2017

Necrotizing autoimmune myopathy.

Christina Liang1, Merrilee Needham

  • 1Department of Neurology, Royal North Shore Hospital, St Leonards, New South Wales, Australia.

Current Opinion in Rheumatology
|September 3, 2011
PubMed
Summary
This summary is machine-generated.

Necrotizing autoimmune myopathy (NAM) is a distinct condition characterized by muscle cell death without significant inflammation. Identifying NAM is crucial for effective treatment, particularly statin-associated cases involving anti-HMGCR antibodies.

More Related Videos

Immunolabelling Myofiber Degeneration in Muscle Biopsies
06:37

Immunolabelling Myofiber Degeneration in Muscle Biopsies

Published on: December 5, 2019

Related Experiment Videos

Last Updated: May 29, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Published on: August 21, 2017

Immunolabelling Myofiber Degeneration in Muscle Biopsies
06:37

Immunolabelling Myofiber Degeneration in Muscle Biopsies

Published on: December 5, 2019

Area of Science:

  • Neurology
  • Immunology
  • Pathology

Background:

  • Necrotizing autoimmune myopathy (NAM) is a newly identified subgroup of idiopathic inflammatory myopathies.
  • Characterized by myocyte necrosis without significant inflammation, despite diverse etiologies.
  • Presents as subacute, severe, symmetrical proximal myopathy with elevated creatine kinase levels.

Purpose of the Study:

  • To define the heterogeneous entity of NAM.
  • Summarize clinical, laboratory, and muscle biopsy findings.
  • Facilitate diagnosis and treatment of NAM.

Main Methods:

  • Review of clinical presentations.
  • Analysis of laboratory findings, including creatine kinase levels.
  • Histopathological examination of muscle biopsies.

Main Results:

  • Statin-associated NAM linked to antibodies against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) protein.
  • HMGCR is upregulated in regenerating muscle fibers.
  • Suggests NAM is antibody-mediated, explaining persistent symptoms post-statin cessation.

Conclusions:

  • Recognizing and distinguishing NAM from other myopathies is essential.
  • NAM has the potential to be amenable to treatment.
  • Anti-HMGCR antibody testing may aid in differentiating immune from non-immune statin myopathies.