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. 2021 Aug 2;8:695952. doi: 10.3389/fcvm.2021.695952

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Copyright © 2021 Tourki and Halade.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Resolvin D1 and lipoxin receptor-deficient mice (FPR2/ALXKO) complement the criteria of HFpEF with profound age-associated endothelial dysfunction and inflammation in the spleen, heart, and kidneys with signs of chronic inflammation. (A) Left panel indicates the heterogeneous, multidimensional, and multiorgan metabolic defects that contribute to HFpEF. (B) Right panel indicates the dysfunction of the resolution receptor FPR2/ALX in mice that develops spontaneous obesity with diastolic dysfunction along with limited changes in systolic function when obesity is superimposed on aging as signs of preserved ejection fraction. Suboptimal inflammation indicated with profound activation of IL1β gene expression in the heart, kidneys, and lungs in FPR2/ALXKO mice exemplifies the age-associated cardiac strain dysfunction, myocardium dissynchronicity, and amplified inflammation. *p < 0.05 compared to control WT group.