What is the clinical evidence from this study?

Study design: Review. Population: Heart failure with preserved ejection fraction (HFpEF).

What does this research mean for the field?

Cardiac macrophage heterogeneity and comorbidity-induced immunometabolic shifts drive HFpEF pathogenesis, presenting subset-specific macrophage targeting as a promising therapeutic strategy. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To review the immunometabolic regulatory mechanisms governing cardiac macrophage heterogeneity in heart failure with preserved ejection fraction (HFpEF) and highlight emerging subset-specific therapeutic strategies.

September 10, 2026Frontiers in ImmunologyOpen Access

Immunometabolic regulation of cardiac macrophages in heart failure with preserved ejection fraction

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Key result

Resident and monocyte-derived cardiac macrophages link immunometabolism to HFpEF pathogenesis and offer subset-specific therapeutic targets.

Why the study?

Targeting specific macrophage subsets offers promising therapeutic avenues in HFpEF, but challenges like off-target effects and clinical translation remain.

Design

Review

Authors

JLJiayun LiangRegenerative Medicine Institute MSManman SuCentral South University RLRenjie LiuJilin University

Discussion

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Implication

Immunometabolic targeting of macrophage subsets merits exploration in HFpEF; hypothesis-generating and requires prospective trials before clinical adoption.

Key Points

To review the immunometabolic regulatory mechanisms governing cardiac macrophage heterogeneity in heart failure with preserved ejection fraction (HFpEF) and highlight emerging subset-specific therapeutic strategies.
Narrative review analyzing the metabolic reprogramming, functional polarization, and crosstalk of cardiac macrophage subpopulations in HFpEF.
Synthesized evidence distinguishing cardiac resident macrophages from monocyte-derived macrophages and their modulation by systemic comorbidity-induced metabolites.
Cardiac resident CCR2- macrophages preserve homeostasis and tissue repair, whereas recruited monocyte-derived CCR2+ macrophages accelerate inflammation, myocardial fibrosis, and diastolic dysfunction.
Comorbidities such as obesity, diabetes, and hypertension cause metabolic perturbations where metabolites including fatty acids, lactate, and succinate drive pro-inflammatory macrophage polarization.
Therapeutic interventions selectively targeting specific macrophage subpopulations show promise for treating HFpEF, though translational hurdles and off-target risks remain.

Structured PICO

Population

Patients with heart failure with preserved ejection fraction (HFpEF) and preclinical murine models of HFpEF

This review elucidates the immunometabolic crosstalk and distinct roles of macrophage subsets in HFpEF, highlighting emerging subset-specific therapeutic strategies.

Limitations

Challenges in clinical translation of macrophage-targeted therapies
Potential for off-target effects
Challenges like off-target effects and clinical translation remain for macrophage-targeted therapies

Cite This Study

Liang et al. (2026) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Cardiac resident macrophages and monocyte-derived macrophages play central roles in linking immunometabolism to HFpEF pathogenesis, offering promising subset-specific therapeutic avenues.

synapsesocial.com/papers/6aa27a5658559d80afc72f49 https://doi.org/10.3389/fimmu.2026.1896936

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Implication

Immunometabolic targeting of macrophage subsets merits exploration in HFpEF; hypothesis-generating and requires prospective trials before clinical adoption.

Immunometabolic regulation of cardiac macrophages in heart failure with preserved ejection fraction

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

Immunometabolic regulation of cardiac macrophages in heart failure with preserved ejection fraction

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

Also Consider

Also Consider