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The secretome of EAT mirrors that of dysfunctional VAT characterized by tumor necrosis factor-alpha, interleukin-6, and their respective soluble receptors [123] So, EAT promoted the development and maintenance of AF through a pro-inflammatory and pro-fibrotic environment [124] leading to autonomic imbalance, connexin dysfunction, cell shortening, increase collagen deposition, and calcium overload [125, 126]

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Additionally, future research should explore the impact of higher doses of semaglutide and its effects independently of concomitant medications to fully understand its potential, he says