Michael Lopez
University of Alabama at Birmingham, AL·Genetics·Early-career
Duchenne muscular dystrophy is an inherited disease in which skeletal muscles gradually waste away. It starts with loss of dystrophin, a protein that stabilizes the muscle cell membrane.
- Fields
Genetics
Physiology
Biology
- Topics
Duchenne muscular dystrophy
dystrophin
skeletal muscle
- Grants
- 1 known grant, through Nov 2026
What they work on
- Test how over-expressing or knocking down Smad8, a TGF-beta–linked transcription factor elevated in Duchenne muscle, changes muscle cell growth, maturation and regeneration in cell culture and Duchenne mouse models.
- Determine how changing Smad8 levels affects myomiRs, muscle-enriched microRNAs that regulate gene expression, and the downstream messenger RNA pathways they control.
- Map the molecular mechanisms by which TGF-beta/Smad8 signaling promotes dystrophic muscle damage through myomiR repression, to identify pathways for potential therapeutic intervention.
More about the research
Without it, membranes become fragile. Much of the damage, however, comes from secondary effects: muscle cells fail to divide, mature and regenerate properly, and inflammation makes these problems worse. Understanding those secondary processes could reveal new ways to slow the disease.
Why it matters
Boys and young men with Duchenne muscular dystrophy lose muscle progressively and have limited treatments. By clarifying how the overactive Smad8 pathway shuts down muscle microRNAs, this work could reveal new therapeutic targets. Those targets might protect muscle regeneration and slow wasting in addition to approaches that address dystrophin loss.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Hongshuai Li
University of Iowa, IA·Physiology
Identify which cells in dystrophic skeletal muscle produce the bone-regulating myokine FGF21 and the molecular signals that switch it on, using DMD mouse models.
Rita Perlingeiro
University of Minnesota, MN·Biomedical Engineering
Determine how the host muscle environment affects engraftment of PSC-derived myogenic progenitors in an immune-deficient FKRP mutant mouse model of dystroglycanopathy.
Renzhi Han
Indiana University-Purdue University-Indianapolis, IN·Pharmacology
Develop an improved triple-vector system in next-generation myotropic adeno-associated virus capsids to reconstitute full-length dystrophin by protein trans-splicing across skeletal, diaphragm, and heart muscle in models of Duchenne muscular dystrophy.
The school
University of Alabama at Birmingham: 45 labs on PI Pages, $866M a year on research, 166 research doctorates a year.
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