Markus Beer
University of Basel
8 Papers
Markus Beer is an academic researcher from University of Basel. The author has contributed to research in topics: Skeletal muscle & Inflammation. The author has an hindex of 7, co-authored 8 publications.
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Papers
The PGC-1 coactivators promote an anti-inflammatory environment in skeletal muscle in vivo.
TL;DR: The anti-inflammatory environment in muscle that is promoted by the PGC-1s might contribute to the beneficial effects of these coactivators on muscle function and provides a molecular link underlying the tight mutual regulation of metabolism and inflammation.
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PGC-1α modulates necrosis, inflammatory response, and fibrotic tissue formation in injured skeletal muscle
Ivana Dinulovic,Regula Furrer,Sabrina Di Fulvio,Arnaud Ferry,Markus Beer,Christoph Handschin +5 more
TL;DR: Interestingly, PGC-1α-dependent effects at the early stages of regeneration are observed, in particular regarding macrophage accumulation and polarization from the pro- inflammatory M1 to the anti-inflammatory M2 type, a faster resolution of necrosis and protection against the development of fibrosis after multiple CTX-induced injuries.
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Paracrine cross-talk between skeletal muscle and macrophages in exercise by PGC-1α-controlled BNP
TL;DR: It is demonstrated that besides a dominant role in controlling cellular metabolism, the peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) also has a profound effect on cytokine expression in muscle tissue.
Muscle PGC-1α modulates satellite cell number and proliferation by remodeling the stem cell niche
TL;DR: Intriguingly, muscle PGC-1α triggers a remodeling of the SC niche by altering the extracellular matrix composition, including the levels of fibronectin, which affects the proliferative output of SCs.
Transcriptional Activation of PPARα by Phenobarbital in the Absence of CAR and PXR
TL;DR: Evidence is provided that phenobarbital directly induces transcription of the PPARalpha gene via its HNF-4alpha response element, and indirectly by lack of inhibitory crosstalk of AMPK, CAR and PXR with HNF -4alpha.
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