Key result
Trem2 deletion worsens cardiac hypertrophy, diastolic dysfunction, and renal injury in hypertensive mice.
Why the study?
The immune system is implicated in cardiac remodelling in HFpEF, but the role of Trem2 in hypertensive heart failure was unknown.
Does genetic deletion of Trem2 worsen cardiac outcomes in a mouse model of hypertensive heart failure?
Does genetic deletion of Trem2 worsen cardiac outcomes in a mouse model of hypertensive heart failure?
Trem2 plays a cardioprotective role in a murine model of hypertensive heart failure, suggesting a potential therapeutic target for HFpEF.
Answers are grounded in this paper and cite their sources.
Trem2 appears cardioprotective in this murine model; hypothesis-generating for HFpEF therapies but should not yet change practice.
AIMS: Heart failure with preserved ejection fraction (HFpEF) is characterized by diastolic dysfunction, microvascular dysfunction, and myocardial fibrosis with recent evidence implicating the immune system in orchestrating cardiac remodelling. METHODS AND RESULTS: Here, we show the mouse model of deoxycorticosterone acetate (DOCA)-salt hypertension induces key elements of HFpEF, including diastolic dysfunction, exercise intolerance, and pulmonary congestion in the setting of preserved ejection fraction. A modified single-cell sequencing approach, cellular indexing of transcriptomes and epitopes by sequencing, of cardiac immune cells reveals an altered abundance and transcriptional signature in multiple cell types, most notably cardiac macrophages. The DOCA-salt model results in differential expression of several known and novel genes in cardiac macrophages, including up-regulation of Trem2, which has been recently implicated in obesity and atherosclerosis. The role of Trem2 in hypertensive heart failure, however, is unknown. We found that mice with genetic deletion of Trem2 exhibit increased cardiac hypertrophy, diastolic dysfunction, renal injury, and decreased cardiac capillary density after DOCA-salt treatment compared to wild-type controls. Moreover, Trem2-deficient macrophages have impaired expression of pro-angiogenic gene programmes and increased expression of pro-inflammatory cytokines. Furthermore, we found that plasma levels of soluble TREM2 are elevated in DOCA-salt treated mice and humans with heart failure. CONCLUSIONS: Together, our data provide an atlas of immunological alterations that can lead to improved diagnostic and therapeutic strategies for HFpEF. We provide our dataset in an easy to explore and freely accessible web application making it a useful resource for the community. Finally, our results suggest a novel cardioprotective role for Trem2 in hypertensive heart failure.
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Smart et al. (2023) studied Heart failure with preserved ejection fraction (HFpEF). Genetic deletion of Trem2 vs. Wild-type controls was evaluated on Cardiac hypertrophy, diastolic dysfunction, renal injury, and cardiac capillary density.
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