June 1, 2014Cardiovascular ResearchOpen Access

CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans

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Structured PICO

Population

Wild-type and CXCR3 null mice undergoing reperfused infarction protocols, and isolated cardiac fibroblasts

Intervention

CXCR3 genetic knockout (in vivo) and CXCL10 treatment (in vitro)

Comparator

Wild-type mice and untreated cells

Outcome

Cardiac remodeling, systolic dysfunction, scar size, collagen deposition, and fibroblast migrationsurrogate

The anti-fibrotic effects of CXCL10 in the healing infarct are CXCR3-independent and mediated through proteoglycan signaling, suggesting CXCR3-defective CXCL10 as a potential targeted anti-fibrotic strategy.

Discussion

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Implication

Does not support CXCR3 modulation post-MI; leaves open proteoglycan signaling as hypothesis-generating anti-fibrotic target in animal models.

Cite This Study

Saxena et al. (2014) studied this question.

synapsesocial.com/papers/6a7dfd331693de70af99b66a https://doi.org/10.1093/cvr/cvu138

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Implication

Does not support CXCR3 modulation post-MI; leaves open proteoglycan signaling as hypothesis-generating anti-fibrotic target in animal models.

CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans

Structured PICO

Discussion

Implication

Cite This Study

CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider