Our study suggests that cytosolic Ca regulation modifies profibrotic
stimulation in FA. We propose the following mechanism for intrinsic profibrotic bias in
human FA fibroblasts: NCX1 downregulation contributes to slower cytosolic Ca
clearance, thereby sustaining Ca-dependent signaling and consequently increased
expression of CCN2 and other profibrotic factors. If validated in FA heart, our findings
would identify NCX1-mediated Ca extrusion in fibroblasts as a potential therapeutic target
to mitigate fibrosis that contributes to lethal cardiomyopathy in FA patients.
Friday, September 25, 2026
Calcium dysregulation amplifies fibrotic responses to TGFβ in human Friedreich's ataxia fibroblasts
Calcium dysregulation amplifies fibrotic responses to TGFβ in human Friedreich's ataxia fibroblasts
Anna Stepanova, Hibiki Kawamata, Giovanni Manfredi
bioRxiv 2026.09.21.753166; doi: doi:10.64898/2026.09.21.753166
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