ArticleThe American journal of pathology2007
Enhanced Na+/H+ exchange activity contributes to the pathogenesis of muscular dystrophy via involvement of P2 receptors.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- CaBiomolecules · 2025Review
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- P2 Receptor Signaling in Motor Units in Muscular Dystrophy.International journal of molecular sciences · 2023Review
- The Donnan-dominated resting state of skeletal muscle fibers contributes to resilience and longevity in dystrophic fibers.The Journal of general physiology · 2022Article
- A Journey with LGMD: From Protein Abnormalities to Patient Impact.The protein journal · 2021Review
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Molecular and Biomechanical Adaptations to Mechanical Stretch in Cultured Myotubes.Frontiers in physiology · 2021Review
- Rimeporide as a first- in-class NHE-1 inhibitor: Results of a phase Ib trial in young patients with Duchenne Muscular Dystrophy.Pharmacological research · 2020Article
- Fast skeletal myofibers of mdx mouse, model of Duchenne muscular dystrophy, express connexin hemichannels that lead to apoptosis.Cellular and molecular life sciences : CMLS · 2016Article
- Pharmacological therapeutics targeting the secondary defects and downstream pathology of Duchenne muscular dystrophy.Expert opinion on orphan drugs · 2016Article
- Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy.Cell death and differentiation · 2015Review
- Na+ dysregulation coupled with Ca2+ entry through NCX1 promotes muscular dystrophy in mice.Molecular and cellular biology · 2014Article
- Article
- Dysferlin and animal models for dysferlinopathy.Journal of toxicologic pathology · 2012Article
- P2X7 purinoceptor alterations in dystrophic mdx mouse muscles: relationship to pathology and potential target for treatment.Journal of cellular and molecular medicine · 2012Article
- Article
- Effects of mechanical over-loading on the properties of soleus muscle fibers, with or without damage, in wild type and mdx mice.PloS one · 2012Article
- Basal release of ATP: an autocrine-paracrine mechanism for cell regulation.Science signaling · 2010Review
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A subset of muscular dystrophy is caused by genetic defects in dystrophin-associated glycoprotein complex. Using two animal models (BIO14.6 hamsters and mdx mice), we found that Na(+)/H(+) exchanger (NHE) inhibitors prevented muscle degeneration. NHE activity was constitutively enhanced in BIO myotubes, as evidenced by the elevated intracellular pH and enhanced (22)Na(+) influx, with activation of putative upstream kinases ERK42/44. NHE inhibitor significantly reduced the increases in baseline intracellular Ca(2+) as well as Na(+) concentration and stretch-induced damage, suggesting that Na(+)(i)-dependent Ca(2+)overload via the Na(+)/Ca(2+) exchanger may cause muscle damage. Furthermore, ATP was found to be released continuously from BIO myotubes in a manner further stimulated by stretching and that the P2 receptor antagonists reduce the enhanced NHE activity and dystrophic muscle damage. These observations suggest that autocrine ATP release may be primarily involved in genesis of abnormal ionic homeostasis in dystrophic muscles and that Na(+)-dependent ion exchangers play a critical pathological role in muscular dystrophy.
Indexed as
Identifiers
What OpenQuestion holds
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.