ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2018
Therapeutic potential of heat shock protein induction for muscular dystrophy and other muscle wasting conditions.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Clinical improvement of DM1 patients reflected by reversal of disease-induced gene expression in blood.BMC medicine · 2022Trial
- LNC_003296 regulates the proliferation and differentiation of ovine myoblasts by modulating the stability of Hsp70.The veterinary quarterly · 2026Article
- Comparative genomic and evolutionary analysis of the heat shock protein gene family in the chicken genome.Animal biotechnology · 2026Article
- Caenorhabditis elegans small heat-shock protein HSP-12.6 has a highly specialized protective function towards muscle thick filaments in vivo.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Sarcopenia and sepsis fuel a self-perpetuating cycle of immunometabolism decline.Frontiers in immunology · 2026Review
- Early Taurine Administration Decreases the Levels of Receptor-Interacting Serine/Threonine Protein Kinase 1 in the Duchenne Mouse ModelBrain sciences · 2025Article
- Extracellular vesicles in cancer cachexia: deciphering pathogenic roles and exploring therapeutic horizons.Journal of translational medicine · 2024Review
- Oleanolic acid alleviates obesity-induced skeletal muscle atrophy via the PI3K/Akt signaling pathway.FEBS open bio · 2024Article
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Review
- Heat Shock Proteins: Important Helpers for the Development, Maintenance and Regeneration of Skeletal Muscles.Muscles (Basel, Switzerland) · 2023Review
- Automatic Text-Mining Approach to Identify Molecular Target Candidates Associated with Metabolic Processes for Myotonic Dystrophy Type 1.International journal of environmental research and public health · 2023Article
- Mechanism of reduced muscle atrophy via ketone body (D)-3-hydroxybutyrate.Cell & bioscience · 2022Article
- Muscle stem cell adaptations to cellular and environmental stress.Skeletal muscle · 2022Review
- Alpha B-Crystallin in Muscle Disease Prevention: The Role of Physical Activity.Molecules (Basel, Switzerland) · 2022Review
- Complexity of skeletal muscle degeneration: multi-systems pathophysiology and organ crosstalk in dystrophinopathy.Pflugers Archiv : European journal of physiology · 2021Review
- General Structural and Functional Features of Molecular Chaperones.Advances in experimental medicine and biology · 2021Article
- Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy.Redox biology · 2021Review
- The nSMase2/Smpd3 gene modulates the severity of muscular dystrophy and the emotional stress response in mdx mice.BMC medicine · 2020Article
- Mechanisms of exercise-induced preconditioning in skeletal muscles.Redox biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy is the most common and severe of the muscular dystrophies, a group of inherited myopathies caused by different genetic mutations leading to aberrant expression or complete absence of cytoskeletal proteins. Dystrophic muscles are prone to injury, and regenerate poorly after damage. Remorseless cycles of muscle fibre breakdown and incomplete repair lead to progressive and severe muscle wasting, weakness and premature death. Many other conditions are similarly characterized by muscle wasting, including sarcopenia, cancer cachexia, sepsis, denervation, burns, and chronic obstructive pulmonary disease. Muscle trauma and loss of mass and physical capacity can significantly compromise quality of life for patients. Exercise and nutritional interventions are unlikely to halt or reverse the conditions, and strategies promoting muscle anabolism have limited clinical acceptance. Heat shock proteins (HSPs) are molecular chaperones that help proteins fold back to their original conformation and restore function. Since many muscle wasting conditions have pathophysiologies where inflammation, atrophy and weakness are indicated, increasing HSP expression in skeletal muscle may have therapeutic potential. This review will provide evidence supporting HSP induction for muscular dystrophy and other muscle wasting conditions.This article is part of the theme issue 'Heat shock proteins as modulators and therapeutic targets of chronic disease: an integrated perspective'.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.