GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE271nnn/GSE271775/suppl/filelist.txtftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE271nnn/GSE271775/suppl/GSE271775_RAW.tarftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE271nnn/GSE271775/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE271775GEOGSEfalseCellular Crosstalk Drives Hypertrophic Cardiomyopathy in LZTR1 DeficiencyLZTR1 deficiency causes Noonan syndrome (NS) and is associated with the manifestation of severe and early-onset hypertrophic cardiomyopathy (HCM). Although paracrine communication is thought to play a critical role in cardiac pathology, little is known about the underlying pathomechanism leading to the development of HCM and cardiac fibrosis in NS. In the present study, we used 2D and 3D iPSC models with LZTR1 deficiency to dissect the impact of non-cardiomyocytes in the development of NS-associated HCM and uncovered a cytokine-mediated intercellular crosstalk, predominantly activated in the disease state, as a major driver of cardiac hypertrophy and cardiac fibrosis.2026/04/02GSE271775GSM8384929GSM8384930GSM8384931GSM8384923GSM8384924GSM8384932GSM8384922GSM8384933GSM8384927GSM8384928GSM8384925GSM838492624676271775Homo sapiens