Key result
Systems biology investigates candidates for liver-heart crosstalk in HFpEF and MASLD.
Why the study?
HFpEF and metabolic dysfunction-associated steatotic liver disease share a metabolic pathogenetic substrate and are directly linked, but systemic molecular dynamics of their interorgan crosstalk remain unclear.
Identifies candidate mediators of liver-heart crosstalk in HFpEF-MASLD; leaves open their causal role and therapeutic relevance.
Heart failure with preserved ejection fraction (HFpEF) accounts for more than half of heart failure cases worldwide.Obesity and metabolic syndrome are major drivers of HFpEF pathophysiology resulting in a complex systemic syndrome with far-reaching clinical implications involving extra-cardiac organs.Owing to their shared metabolic pathogenetic substrate, accumulating evidence support that HFpEF, and metabolic dysfunction-associated steatotic liver disease (MASLD)/nonalcoholic fatty liver disease (NAFLD) do not simply co-exist but are directly linked.
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Strocchi et al. (2024) studied Heart failure with preserved ejection fraction (HFpEF). A systems biology approach was used to investigate candidates for liver-heart interorgan crosstalk in heart failure with preserved ejection fraction and metabolic dysfunction-associated steatotic liver disease.
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