GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336017/primaryOK200TranscriptomicsRattus norvegicusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336017GEOGSEfalseSIRT7 acts as a core regulator in resveratrol-mediated gene transcription to alleviate diabetic cardiomyopathy.Diabetic cardiomyopathy (DCM), a severe diabetic complication manifesting as myocardial hypertrophy, oxidative stress, cardiomyocyte apoptosis and extracellular matrix (ECM) remodeling, lacks effective therapeutic interventions. Resveratrol (Res) confers cardioprotection, and SIRT7 participates in high-glucose (HG)-elicited myocardial damage. This study aimed to clarify whether Res-activated SIRT7 modulates transcriptional profiles to counteract HG-induced DCM lesions. HG-challenged cardiomyocytes and diabetic mouse models were established; a SIRT7 inhibitor was administered to verify the underlying mechanism. Transcriptome sequencing was conducted to identify pivotal functional genes, followed by GO and KEGG enrichment analyses. Immunofluorescence, western blot and multiple histopathological staining assays were adopted to assess oxidative stress, apoptosis, myocardial hypertrophy and cardiac fibrosis. HG exposure boosted reactive oxygen species (ROS) production, facilitated cardiomyocyte apoptosis, increased hypertrophy-related protein levels, and dysregulated genes linked to inflammation and ECM remodeling. Res treatment upregulated SIRT7, rescued all HG-triggered pathological phenotypes, and modulated PI3K-Akt, NF-κB and Hippo signaling cascades. Notably, pharmacological suppression of SIRT7 completely abrogated Res-elicited cardioprotection. Res ameliorates HG-induced DCM through SIRT7-dependent transcriptional reprogramming, which offers promising molecular targets for DCM treatment.2026/07/01GSE336017GSM9825267GSM9825268GSM9825269GSM9825263GSM9825264GSM9825265GSM9825266GSM9825270GSM9825271GSM9825260GSM9825261GSM982526225947336017Rattus norvegicus