NIH R01 · 2024
Connexin 43: a new player in Duchenne muscular dystrophy associated cardiomyopathy
SUMMARY Duchenne muscular dystrophy (DMD) is incurable. Lack of dystrophin is the culprit. While the ultimate solution to this devastating disease is to restore dystrophin, the scientific and medical communities actively seek to discover and fix key secondary factors. We study a corrective role of phosphorylated Connexin-43 (Cx43) as a potential secondary factor in DMD cardiomyopathy. Cx43 forms gap junction channels at the intercalated disc (ID) of the cardiomyocytes (CMs). The gap junction helps the heart to beat in unison. We found that dystrophic CMs exhibit pathological Cx43 remodeling – that is Cx43 lateralization away from the ID. Lateralized Cx43 proteins remain as hemichannels,…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.