ArticleClinical and translational medicine2026
Macrophage Cluster of Differentiation 163 promotes post-infarction cardiac repair and preserves left ventricular function via osteopontin.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCardiac macrophages (cMacs) have been implicated in myocardial repair following myocardial infarction (MI), yet their therapeutic potential in ischaemic cardiomyopathy (ICM) remains limited by an incomplete understanding of their molecular regulation. Cluster of Differentiation 163 (CD163) is highly expressed in these macrophages, yet its functional role in regulating post-MI cardiac repair remains unknown.
methodsA cross-sectional clinical study was conducted to assess the association between circulating soluble CD163 concentration and heart failure due to ICM. To investigate the functional contribution of CD163 in ICM, wild-type (WT) and Cd163
resultsCirculating soluble CD163 levels were markedly elevated in patients with ICM-induced heart failure compared with individuals without heart failure (median difference 34.5 ng/mL, IQR 13.6-54.6 ng/mL, p = .002) and showed a positive correlation with the extent of systolic dysfunction and left ventricular (LV) dilation. Cd163
conclusionsIn cMacs, CD163 contributes to post-MI repair by upregulating OPN expression, which in turn helps maintain systolic function. KEY POINTS: Soluble CD163 is elevated in ICM and correlates with LV dysfunction. Cd163
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