Ischemic stroke induces cardiac dysfunction and alters transcriptome profile in mice

Background Stroke can induce cardiac dysfunction in the absence of primary cardiac disease; however, the mechanisms underlying the interaction between the neurological deficits and the heart are poorly understood. The objective of this study was to investigate the effects of stroke on cardiac function and to identify the transcriptome characteristics of the heart. Results Stroke significantly decreased heart weight/tibia length ratio and cardiomyocyte cross-sectional areas and increased atrogin-1 and the E3 ubiquitin ligase MuRF-1, indicating myocardial atrophy in MCAO-induced mouse hearts. RNA sequencing of mRNA revealed 383 differentially expressed genes (DEGs) in MCAO myocardium, of which 221 were downregulated and 162 upregulated. Grouping of DEGs based on biological function and quantitative PCR validation indicated that suppressed immune response and collagen synthesis and altered activity of oxidoreductase, peptidase, and endopeptidase may be involved in MCAO-induced cardiomyopathy. The DEGs were mainly distributed in the membrane or extracellular region of cardiomyocytes and acted as potential mediators of stroke-induced cardiac dysregulation involved in cardiac atrophy. Conclusion Stroke induced a unique transcriptome response in the myocardium and resulted in immediate cardiac atrophy and dysfunction.

Automated summary

Stroke can lead to immediate cardiac atrophy and dysfunction, as indicated by decreased heart weight and cardiomyocyte cross-sectional areas, and increased expression of certain genes involved in myocardial atrophy. RNA sequencing identified differentially expressed genes related to immune response suppression, collagen synthesis inhibition, and altered enzyme activity in stroke-induced cardiomyopathy. These genes are mainly located in the membrane or extracellular region of cardiomyocytes and may serve as potential mediators in the dysregulation of stroke-induced cardiac function.