U01.17.011 Duchenne Muscular Dystrophy (DMD): Genetics and Clinical Hallmarks

Master Duchenne Muscular Dystrophy (U01.17.011) for USMLE Step 1. Learn about dystrophin frameshift mutations, Gowers sign, and the causes of pseudohypertrophy. High-yield guide on mymedschool.org.

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D言語の更新まとめ 2026年1月版（dmd 2.112.0） - Qiita

はじめに D言語の公式コンパイラである dmd が更新され、最新バージョンである 2.112.0 が 2026/01/07 にリリースされました。 今回もmacOSのRegression騒ぎやらで色々あったようで、前回リリースの 2.111.0 からかなりの時間を要しまし...

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CD4+ T cells fuel the Duchenne cardiomyopathy

Duchenne muscular dystrophy (DMD) is a X-linked genetic disorder, in which cardiomyopathy represents a major cause of mortality. Although myocardial inflammation and fibrosis are hallmarks of the disease, the role of adaptive immunity in cardiac pathology remains poorly defined. Using the Mdx mouse model, we demonstrate that T and B lymphocytes accumulate in the heart and that activation occurs in heart-draining lymph nodes at an early disease stage. Mdx mice lacking adaptive immunity (Mdx-Scid) were protected from myocardial fibrosis and hypertrophic remodeling. Single-cell RNA sequencing revealed expansion of an inflammatory, matrisome-associated macrophage subset in Mdx but not Mdx-Scid hearts. Genetic deficiency or depletion of CD4⁺ T cells reduced left ventricular fibrosis and preserved systolic function. Moreover, adoptive transfer of T cells von Mdx mice induced myocardial fibrosis and dysfunction in healthy recipients. Our results identify autoreactive CD4⁺ T cells as key drivers of DMD-associated cardiomyopathy and suggest targeted modulation of adaptive immune responses as a potential therapeutic approach in DMD. ### Competing Interest Statement The authors have declared no competing interest. Deutsche Forschungsgemeinschaft, 453989101, 449933847 German Heart Research Foundation, https://ror.org/02yjb3a91, F/02/16