ReviewCurrent opinion in cell biology2007
Dysferlin and muscle membrane repair.
Review in Current opinion in cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 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
118 citing papers in PubMed, 275 citations in OpenAlex.
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Proteomic Profiling of Myofiber Repair Annexins and Their Role in Duchenne Muscular Dystrophy.Proteomics · 2026Review
- Review
- Generation of a novel Dysferlin microdeletion knock-in mouse model mimicking muscular dystrophy-like pathology.Scientific reports · 2026Article
- Dysferlin stabilizes membrane nanodomains of cardiomyocytes after myocardial infarction.Scientific reports · 2026Article
- Dysferlin and the Regulation of CaCells · 2025Review
- Structural insights into lipid membrane binding by human ferlins.The EMBO journal · 2025Article
- Inducing mechanical self-healing in polymer glasses.Nature communications · 2025Article
- Metabolic dysregulation contributes to the development of dysferlinopathy.Life science alliance · 2025Article
- Mechanotransduction and Skeletal Muscle Atrophy: The Interplay Between Focal Adhesions and Oxidative Stress.International journal of molecular sciences · 2025Review
- Review
- Muscular Dystrophies.Advances in experimental medicine and biology · 2025Review
- Silencing AHNAK promotes nasopharyngeal carcinoma progression by upregulating the ANXA2 protein.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Limb Girdle Muscular Dystrophy Type 2B (LGMD2B): Diagnosis and Therapeutic Possibilities.International journal of molecular sciences · 2024Review
- A novel homozygous variant (c.5876T > C: p. Leu1959Pro) in DYSF segregates with limb-girdle muscular dystrophy: a case report.BMC musculoskeletal disorders · 2024Article
- The Dysferlinopathies Conundrum: Clinical Spectra, Disease Mechanism and Genetic Approaches for Treatments.Biomolecules · 2024Review
- Extracellular matrix contribution to disease progression and dysfunction in myopathy.American journal of physiology. Cell physiology · 2023Review
- Pharmacotherapeutic Approaches to Treatment of Muscular Dystrophies.Biomolecules · 2023Review
- Structural basis for TRIM72 oligomerization during membrane damage repair.Nature communications · 2023Article
- Role of calcium-sensor proteins in cell membrane repair.Bioscience reports · 2023Review
58 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ability to repair membrane damage is conserved across eukaryotic cells and is necessary for the cells to survive a variety of physiological and pathological membrane disruptions. Membrane repair is mediated by rapid Ca(2+)-triggered exocytosis of various intracellular vesicles, such as lysosomes and enlargeosomes, which lead to the formation of a membrane patch that reseals the membrane lesion. Recent findings suggest a crucial role for dysferlin in this repair process in muscle, possibly as a Ca(2+) sensor that triggers vesicle fusion. The importance of membrane repair is highlighted by the genetic disease, dysferlinopathy, in which the primary defect is the loss of Ca(2+)-regulated membrane repair due to dysferlin deficiency. Future research on dysferlin and its interacting partners will enhance the understanding of this important process and provide novel avenues to potential therapies.
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.