Maladaptive lipid partitioning in obesity-related heart failure with preserved ejection fraction: From depot dysfunction to metabolic phenotyping

Figure 1 Maladaptive lipid-partitioning framework in obesity-related heart failure with preserved ejection fraction. Human studies support depot-specific adiposity, myocardial metabolic abnormalities, and selected clinical associations, whereas several linking mechanisms remain unproven in humans. Solid arrows denote reported human observational or interventional associations and do not imply a single proven causal sequence. Dashed arrows denote hypothesis-generating mechanistic links without proven human causality. VAT: Visceral adipose tissue; MASLD: Metabolic dysfunction-associated steatotic liver disease; EAT: Epicardial adipose tissue; PVAT: Perivascular adipose tissue; TNF-α: Tumor necrosis factor-α; IL-6: Interleukin-6; MCP-1: Monocyte chemoattractant protein-1; DAG: Diacylglycerol; BCAA: Branched-chain amino acid; TCA: Tricarboxylic acid; HFpEF: Heart failure with preserved ejection fraction.