The State of the Art of Piezo1 Channels in Skeletal Muscle Regeneration

Piezo1 channels are highly mechanically-activated cation channels that can sense and transduce the mechanical stimuli into physiological signals in different tissues including skeletal muscle. In this focused review, we summarize the emerging evidence of Piezo1 channel-mediated effects in the physio...

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Published inInternational journal of molecular sciences Vol. 23; no. 12; p. 6616
Main Authors Bernareggi, Annalisa, Bosutti, Alessandra, Massaria, Gabriele, Giniatullin, Rashid, Malm, Tarja, Sciancalepore, Marina, Lorenzon, Paola
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 14.06.2022
MDPI
Subjects
Aging
Channel gating
Mechanical stimuli
Muscles
Musculoskeletal system
myoblasts
Myogenesis
myotubes
Permeability
Piezo1
Population
Review
Sarcopenia
satellite cells
Skeletal muscle
Vascularization
Yoda1
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Summary:Piezo1 channels are highly mechanically-activated cation channels that can sense and transduce the mechanical stimuli into physiological signals in different tissues including skeletal muscle. In this focused review, we summarize the emerging evidence of Piezo1 channel-mediated effects in the physiology of skeletal muscle, with a particular focus on the role of Piezo1 in controlling myogenic precursor activity and skeletal muscle regeneration and vascularization. The disclosed effects reported by pharmacological activation of Piezo1 channels with the selective agonist Yoda1 indicate a potential impact of Piezo1 channel activity in skeletal muscle regeneration, which is disrupted in various muscular pathological states. All findings reported so far agree with the idea that Piezo1 channels represent a novel, powerful molecular target to develop new therapeutic strategies for preventing or ameliorating skeletal muscle disorders characterized by an impairment of tissue regenerative potential.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms23126616