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“the adipokine hypothesis does not eliminate the complexity of HFpEF, but it contributes to organize it. It invites a transition from treating volume to treating signal; from reacting to dysfunction to intercepting it upstream. If this vision holds, it may reorient how we approach HFpEF as well as a broader class of cardiometabolic diseases defined not by cardiac origin but by cardiac consequence. Caution is warranted, however. As with all translational frameworks, testing across human cohorts with broad geographic, genetic, and phenotypic diversity remains essential.”
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Gabriele G. Schiattarella (2025) studied this question.
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