ArticleNeurobiology of aging2011
Altered Ca2+ homeostasis in the skeletal muscle of DJ-1 null mice.
Article in Neurobiology of aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular Mechanisms and Therapeutic Potential of DJ-1 in Skeletal Muscle Homeostasis and Disease.Comprehensive Physiology · 2026Review
- Mitochondrial dysfunction in Parkinson's disease - a key disease hallmark with therapeutic potential.Molecular neurodegeneration · 2023Review
- Balancing ER-Mitochondrial CaTrends in cell biology · 2021Review
- DJ-1 regulates the integrity and function of ER-mitochondria association through interaction with IP3R3-Grp75-VDAC1.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Cardioprotective effects of CuScientific reports · 2016Article
- Differences in strength-duration curves of electrical diagnosis by physiotherapists between DJ-1 homozygous knockout and wild-type mice: a randomized controlled pilot trial.Journal of physical therapy science · 2016Article
- Muscle-Specific Myosin Heavy Chain Shifts in Response to a Long-Term High Fat/High Sugar Diet and Resveratrol Treatment in Nonhuman Primates.Frontiers in physiology · 2016Article
- DJ-1 links muscle ROS production with metabolic reprogramming and systemic energy homeostasis in mice.Nature communications · 2015Article
- Mitochondrial Ca(2+) and neurodegeneration.Cell calcium · 2012Review
- Calcium homeostasis in aging neurons.Frontiers in genetics · 2012Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Loss-of-function mutations in DJ-1 are associated with early-onset of Parkinson's disease. Although DJ-1 is ubiquitously expressed, the functional pathways affected by it remain unresolved. Here we demonstrate an involvement of DJ-1 in the regulation of Ca(2+) homeostasis in mouse skeletal muscle. Using enzymatically dissociated flexor digitorum brevis muscle fibers from wild-type (wt) and DJ-1 null mice, we examined the effects of DJ-1 protein on resting, cytoplasmic [Ca(2+)] ([Ca(2+)](i)) and depolarization-evoked Ca(2+) release in the mouse skeletal muscle. The loss of DJ-1 resulted in a more than two-fold increase in resting [Ca(2+)](i). While there was no alteration in the resting membrane potential, there was a significant decrease in depolarization-evoked Ca(2+) release from the sarcoplasmic reticulum in the DJ-1 null muscle cells. Consistent with the role of DJ-1 in oxidative stress regulation and mitochondrial functional maintenance, treatments of DJ-1 null muscle cells with resveratrol, a mitochondrial activator, or glutathione, a potent antioxidant, reversed the effects of the loss of DJ-1 on Ca(2+) homeostasis. These results provide evidence of DJ-1's association with Ca(2+) regulatory pathways in mouse skeletal muscle, and suggest the potential benefit of resveratrol to functionally compensate for the loss of DJ-1.
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