Subepicardial adipose genes contribute to the deterioration of heart failure preserved ejection fraction

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background The mortality of patients with acute myocardial infarction (MI) raised rapidly in last decade and obesity are becoming the major cause to CAD progression, thus inducing heart failure preserved ejection fraction (HFpEF). However, why visceral adipocytes show different effects on healthy and ageing cardiomyocytes is less known. Methods GSE251971 was downloaded and Venn diagram between visceral adipocyte genes genes and DEGs was performed to obtain visceral adipocyte-associated DEGs in heart failure. Protein-protein interaction (PPI) network was constructed to obtain the hub genes utilizing the Cytoscape plugin Cytohubba. The hub genes and their interactions were analyzed using NetworkAnalyst 3.0 and for validation, the hub genes expressions were analyzed using Single-cell sequencing data, cell lines and human sub-epicardial tissues and blood samples. Results Using Venn diagram, 71 visceral adipocyte-associated DEGs were identified. Nine hub genes were obtained, including OGN, SELL, FOS, NKG7, LOX, HBB, CXCL9, CP and ALOX5. Single-cell sequencing demonstrated all hub genes were highly expressed in human hypertrophic cardiomyopathy and ischemic cardiomyopathy patients with end-stage heart failure. The related OGN, FOS, NKG7 and ALOX5 mRNA expressions were significantly highly expressed in sub-epicardial tissues in HFpEF patients. AUCs of OGN, FOS and ALOX5 were 0.902, 0.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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