CXCL5–CXCR2 axis mediates myocardial ischemia/reperfusion injury by inducing infiltration of myeloid-derived macrophages and neutrophils

Q: What is the clinical evidence from this study?

Population: Myocardial ischemia/reperfusion (MI/R) injury. Intervention: Genetic deletion of CXCL5, myeloid-specific deletion of CXCR2, and pharmacological blockade of CXCR2.

Jiao Fang; Pang‐Bo Li; Yun-Long Zhang; Hui‐Hua Li

doi:10.1016/j.intimp.2026.117267

August 11, 2026International ImmunopharmacologyOpen Access

CXCL5–CXCR2 axis mediates myocardial ischemia/reperfusion injury by inducing infiltration of myeloid-derived macrophages and neutrophils

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Key result

Targeting the CXCL5-CXCR2 axis shows preclinical promise against myocardial ischemia-reperfusion injury and early post-infarct remodeling.

Why the study?

The roles of CXCL5 and its receptor CXCR2 in myocardial ischemia/reperfusion injury remained unknown.

Does genetic deletion or pharmacological blockade of the CXCL5-CXCR2 axis reduce myocardial ischemia/reperfusion injury in preclinical models?

Key Points

This study aimed to clarify the role of the CXCL5-CXCR2 axis in myocardial ischemia/reperfusion injury.
Genetic deletion of CXCL5 and myeloid-specific deletion of CXCR2 were performed.
Pharmacological blockade of CXCR2 was employed to evaluate its functional significance.
Cardiac function assessed by echocardiography and myocardial damage measured by histological staining.
CXCL5 and CXCR2 expression were elevated in response to myocardial ischemia/reperfusion.
Infiltration of myeloid-derived macrophages and neutrophils was significantly increased.
Targeting the CXCL5-CXCR2 axis reduced myocardial infarct size and improved cardiac function.

Structured PICO

Does genetic deletion or pharmacological blockade of the CXCL5-CXCR2 axis reduce myocardial ischemia/reperfusion injury in preclinical models?

P

Population

Preclinical models of myocardial ischemia/reperfusion (MI/R) injury

I

Intervention

Genetic deletion of CXCL5, myeloid-specific deletion of CXCR2, and pharmacological blockade of CXCR2

O

Outcome

Cardiac function, myocardial infarct size, apoptosis, and fibrosissurrogate

The CXCL5-CXCR2 axis mediates myocardial ischemia/reperfusion injury by inducing infiltration of myeloid-derived macrophages and neutrophils, representing a potential therapeutic target.

Implication

Suggests CXCL5-CXCR2 involvement in MI/R injury; leaves open therapeutic targeting pending validation.

Graphical abstract published by International Immunopharmacology — Graphical abstract · Published by International Immunopharmacology · CC BY 4.0

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Cite This Study

Fang et al. (2026) studied Myocardial ischemia/reperfusion (MI/R) injury. Genetic deletion of CXCL5, myeloid-specific deletion of CXCR2, and pharmacological blockade of CXCR2 was evaluated. Targeting the CXCL5-CXCR2 axis represents a promising therapeutic strategy for myocardial ischemia/reperfusion injury and early post-infarct remodeling.

synapsesocial.com/papers/6a7c3d7806a85aed514b7cec https://doi.org/10.1016/j.intimp.2026.117267

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CXCL5–CXCR2 axis mediates myocardial ischemia/reperfusion injury by inducing infiltration of myeloid-derived macrophages and neutrophils

Key Points

Structured PICO

Implication

Discussion

Cite This Study

CXCL5–CXCR2 axis mediates myocardial ischemia/reperfusion injury by inducing infiltration of myeloid-derived macrophages and neutrophils

Key Points

Structured PICO

Implication

Discussion

Cite This Study

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