ArticleHuman molecular genetics2018
Sarcolipin deletion in mdx mice impairs calcineurin signalling and worsens dystrophic pathology.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Effects of electromyostimulation on sarcolipin and CaBiochemistry and biophysics reports · 2026Article
- Sarcolipin but not phospholamban responds toFrontiers in physiology · 2026Article
- HUWE1 in Skeletal Muscle Prevents Muscle Fatigue via Maintaining Iron and Calcium Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Allosteric Modulation of SERCA Pumps in Health and Disease: Structural Dynamics, Posttranslational Modifications, and Therapeutic Potential.Journal of molecular biology · 2025Review
- The tumor suppressor pRb and its relative p130 are required to maintain murine adult skeletal muscle homeostasis.Oncogene · 2025Article
- Analysis of ATG4C functionAutophagy · 2023Article
- Dwarf Open Reading Frame (DWORF) Gene Therapy Ameliorated Duchenne Muscular Dystrophy Cardiomyopathy in Aged mdx Mice.Journal of the American Heart Association · 2023Article
- 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
- Skeletal and cardiac muscle calcium transport regulation in health and disease.Bioscience reports · 2022Review
- Histological Methods to Assess Skeletal Muscle Degeneration and Regeneration in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Review
- Sarco(endo)plasmic reticulum CaiScience · 2022Article
- Heterozygous SOD2 deletion selectively impairs SERCA function in the soleus of female mice.Physiological reports · 2022Article
- Reducing sarcolipin expression improves muscle metabolism inAmerican journal of physiology. Cell physiology · 2022Article
- Sarcoplasmic Reticulum from Horse Gluteal Muscle Is Poised for Enhanced Calcium Transport.Veterinary sciences · 2021Article
- Characterizing SERCA Function in Murine Skeletal Muscles after 35-37 Days of Spaceflight.International journal of molecular sciences · 2021Article
- Sarcolipin haploinsufficiency prevents dystrophic cardiomyopathy inAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- Is Upregulation of Sarcolipin Beneficial or Detrimental to Muscle Function?Frontiers in physiology · 2021Article
- Sarcolipin Exhibits Abundant RNA Transcription and Minimal Protein Expression in Horse Gluteal Muscle.Veterinary sciences · 2020Article
- Systemic Glycosaminoglycan Clearance by HARE/Stabilin-2 Activates Intracellular Signaling.Cells · 2020Review
- Activation of sarcolipin expression and altered calcium cycling inBiochemistry and biophysics reports · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is the most severe form of muscular dystrophy affecting 1 in 3500 live male births. Although there is no cure for DMD, therapeutic strategies aimed at enhancing calcineurin signalling and promoting the slow fibre phenotype have shown promise in mdx mice, which is the classical mouse model for DMD. Sarcolipin (SLN) is a small protein that regulates the sarco(endo)plasmic reticulum Ca2+-ATPase pump and its expression is highly upregulated in dystrophic skeletal muscle. We have recently shown that SLN in skeletal muscle amplifies calcineurin signalling thereby increasing myofibre size and the slow fibre phenotype. Therefore, in the present study we sought to determine the physiological impact of genetic Sln deletion in mdx mice, particularly on calcineurin signalling, fibre-type distribution and size and dystrophic pathology. We generated an mdx/Sln-null (mdx/SlnKO) mouse colony and hypothesized that the soleus and diaphragm muscles from these mice would display blunted calcineurin signalling, smaller myofibre sizes, an increased proportion of fast fibres and worsened dystrophic pathology compared with mdx mice. Our results show that calcineurin signalling was impaired in mdx/SlnKO mice as indicated by reductions in utrophin, stabilin-2 and calcineurin expression. In addition, mdx/SlnKO muscles contained smaller myofibres, exhibited a slow-to-fast fibre-type switch that corresponded with reduced expression of mitochondrial proteins and displayed a worsened dystrophic pathology compared with mdx muscles. Altogether, our findings demonstrate a critical role for SLN upregulation in dystrophic muscles and suggest that SLN can be viewed as a potential therapeutic target.
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