Anne Bigot

This study identifies age-related changes in the muscle secretome that impair stem cell function through sphingolipid metabolism alterations.

The paper identifies an IL-6-associated SAA axis linked to muscle wasting and poor survival in cancer cachexia through plasma proteomics and functional studies.

This study shows that declining NOX4 in skeletal muscle with age disrupts NFE2L2 adaptive homeostasis, leading to muscle dysfunction and systemic aging, which can be mitigated by sulforaphane or exercise.

The paper identifies EMILIN1 as a TGFβ/SETDB1-regulated secreted biomarker in DMD, showing its role in fibrosis and myogenesis through proteomic analysis of patient-derived myotubes.

This paper develops a 3D human muscle model from DM1 patient myoblasts that recapitulates CLCN1 mis-splicing and myotonia, and tests therapeutic responses.

The paper shows that inhibiting SUMOylation with TAK981 increases DUX4 expression in human muscle cells without affecting DNA methylation or SMCHD1 activity, suggesting a new therapeutic approach for FSHD.

This study shows that SMN loss in SMA Type II myoblasts causes genomic stress, leading to DNA damage and innate immune activation, which impairs myoblast differentiation.

The paper shows mini-agrin prevents calcium leakage and restores the dystrophin complex in dystrophic muscle cells by stabilizing CaV1.1 and reconstituting dystrophin complex components.

This study identifies collagen VI as a conserved pro-fibrotic factor that impairs muscle regeneration in three distinct human myopathies.

This paper develops a cell-based platform to quantify DMPK and MBNL1 in DM1 models and evaluates therapeutic strategies targeting DMPK.

This study identifies bazedoxifene as a potential treatment for LGMD R2 through high-throughput screening of drugs targeting dysferlin aggregation.

This study shows that clathrin plaques and dynamin 2 anchor desmin intermediate filaments and regulate YAP signaling in skeletal muscle in response to mechanical cues.

This study shows that Cav3 mutations in human dystrophic myotubes impair caveolae function, leading to defective mechanoprotection and aberrant IL6/STAT3 signaling.