What is the clinical evidence from this study?

Study design: Case-Control. Population: Acute myocardial infarction (n=243). Intervention: Elevated IL-15 levels vs. Non-CAD controls. Primary outcome: Acute myocardial infarction (aOR 1.320, 95% CI 1.130-1.542, p=<0.001).

What does this research mean for the field?

Interleukin-15 (IL-15) exacerbates cardiac ischemic injury following acute myocardial infarction by impairing macrophage efferocytosis, promoting inflammatory M1 polarization, and enhancing glycolytic activity. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine the mechanistic and pathological role of interleukin-15 (IL-15) in acute myocardial infarction, focusing on macrophage efferocytosis, polarization, and metabolic reprogramming.

July 5, 2026Journal of Zhejiang University SCIENCE B

IL-15 aggravates cardiac ischemic injury via impairing macrophage efferocytosis and driving inflammation

Q: What are the key findings of this study?

Elevated plasma IL-15 levels were significantly associated with an increased risk of acute myocardial infarction (aOR 1.320).

Q: What does this research mean for the field?

Interleukin-15 (IL-15) exacerbates cardiac ischemic injury following acute myocardial infarction by impairing macrophage efferocytosis, promoting inflammatory M1 polarization, and enhancing glycolytic activity. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To determine the mechanistic and pathological role of interleukin-15 (IL-15) in acute myocardial infarction, focusing on macrophage efferocytosis, polarization, and metabolic reprogramming.

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Key result

Elevated plasma IL-15 is linked to ~32% higher risk of acute myocardial infarction.

aOR 1.320
95% CI 1.130-1.542
P<0.001
n=243

Why the study?

While interleukin-15 (IL-15) has been implicated in immune regulation, its precise role in the pathogenesis of acute myocardial infarction has not been clarified.

Does IL-15 deletion or inhibition improve myocardial recovery and reduce inflammation following acute myocardial infarction?

Population

AMI patients and murine models

Comparison

IL-15 and IL-15 receptor α knockout vs control

Design

Preclinical translational and mechanistic study

Authors

LGLei GuoSecond Affiliated Hospital of Zhejiang University ZYZhehui YinPeking University NZNing ZhangHangzhou First People's Hospital

Discussion

Member takes

Implication

IL-15 may worsen AMI injury via macrophage dysfunction; hypothesis-generating in animal models, clinical trials needed.

Key Points

To determine the mechanistic and pathological role of interleukin-15 (IL-15) in acute myocardial infarction, focusing on macrophage efferocytosis, polarization, and metabolic reprogramming.
Quantified plasma IL-15 concentrations in patients with acute myocardial infarction (n=121) and non-coronary artery disease controls (n=122).
Evaluated myocardial inflammation, apoptosis, and cardiac functional remodeling across baseline, 3, 7, and 14 days post-infarction using IL-15 knockout and IL-15 receptor α (IL-15Rα) knockout mouse models.
Assessed bone marrow-derived macrophages and MERTK-overexpressing RAW 264.7 cells treated with recombinant murine IL-15 to evaluate NF-κB activation, efferocytosis capacity, and glycolytic gene expression.
Plasma IL-15 levels were significantly higher in acute myocardial infarction patients (11.42±3.53 pg/mL) than non-coronary artery disease controls (2.43±1.10 pg/mL, P<0.001), independently associating with infarction risk (aOR 1.320, 95% CI 1.130–1.542, P<0.001).
Genetic knockout of either IL-15 or IL-15Rα significantly reduced cardiac apoptosis and tissue inflammation while preserving left ventricular ejection fraction and limiting infarct size in mice.
IL-15 suppressed macrophage efferocytosis by downregulating Mer tyrosine kinase (MERTK), stimulated pro-inflammatory M1 polarization via NF-κB p65 phosphorylation, and increased glycolytic pathway flux.

Study Design

Type

Case-Control (n=243)

Structured PICO

Does IL-15 deletion or inhibition improve myocardial recovery and reduce inflammation following acute myocardial infarction?

Population

243 patients, including 121 with acute myocardial infarction and 122 non-coronary artery disease controls, evaluated for the association between plasma IL-15 levels and AMI.

Exposure

Genetic deletion of IL-15 or IL-15Rα, or administration of recombinant murine IL-15.

Comparator

Wild-type mice, non-CAD human controls, or vehicle (PBS) treatment.

Outcome

Cardiac inflammation, apoptosis, macrophage efferocytosis, and myocardial function (LVEF, FS) following AMI.surrogate

Main Result

Odds Ratio: 1.32 (95% CI 1.13–1.542)

p-value: p=<0.001

IL-15 exacerbates cardiac ischemic injury by impairing macrophage efferocytosis and promoting inflammation, suggesting it may be a therapeutic target for myocardial recovery post-AMI.

Limitations

Not explicitly stated in the provided text

Cite This Study

Guo et al. (2026) conducted a case-control in Acute myocardial infarction (n=243). Elevated IL-15 levels vs. Non-CAD controls was evaluated on Acute myocardial infarction (aOR 1.320, 95% CI 1.130-1.542, p=<0.001). Elevated plasma IL-15 levels were significantly associated with an increased risk of acute myocardial infarction (aOR 1.320).

synapsesocial.com/papers/6a49f3b0f5d1d45b287ffafe https://doi.org/10.1631/jzus.b2500477

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IL-15 aggravates cardiac ischemic injury via impairing macrophage efferocytosis and driving inflammation

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Main Result

Limitations

Cite This Study

IL-15 aggravates cardiac ischemic injury via impairing macrophage efferocytosis and driving inflammation

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Main Result

Limitations

Cite This Study

Also Consider

Also Consider