Publications by authors named "Iteoluwakishi H Gamu"
Article Synopsis
- The absence of dystrophin protein in boys with Duchenne Muscular Dystrophy (DMD) leads to heart problems, but common mouse models don't show these issues until they are older, making it hard to study early cardiac effects.
- The mdx mouse model with a DBA/2J genetic background (D2-) demonstrates early heart dysfunction, revealing increased inflammation and fibrosis as key contributors to juvenile cardiomyopathy.
- Activating the N-formyl peptide receptor 2 (FPR2) can reduce chronic inflammation and fibrosis, offering a potential new treatment strategy to prevent heart problems in young D2-mdx mice with DMD.
Lack of dystrophin expression is the underlying genetic basis for Duchenne muscular dystrophy (DMD). However, disease severity varies between patients, based on specific genetic modifiers. D2-mdx is a model for severe DMD that exhibits exacerbated muscle degeneration and failure to regenerate even in the juvenile stage of the disease.
View Article and Find Full Text PDFLack of dystrophin is the genetic basis for the Duchenne muscular dystrophy (DMD). However, disease severity varies between patients, based on specific genetic modifiers. D2- is a model for severe DMD that exhibits exacerbated muscle degeneration and failure to regenerate even in the juvenile stage of the disease.
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