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Research indicates that excessively hyperplastic and dysfunctional EAT exerts adverse cardiac effects primarily through two pathways: first, by serving as a source of pro-inflammatory mediators, and second, through direct cardiac mechanical effects, ultimately promoting cardiovascular disease (82)

Patients who developed one of these conditions before follow-up BMI measurements were excluded

Individuals with the infantile hepatocardiomuscular form of the disease are often compound heterozygotes

Overlooking FDA requirements

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Lymphatic vascular defects promoted by Prox1 haploinsufficiency cause adult-onset obesity