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Corrigendum
Open Access | 
10.1172/JCI205881
Corrigendum to Angiopoietin-2 exacerbates cardiac hypoxia and inflammation after myocardial infarction
Seung-Jun Lee, Choong-kun Lee, Seok Kang, Intae Park, Yoo Hyung Kim, Seo Ki Kim, Seon Pyo Hong, Hosung Bae, Yulong He, Yoshiaki Kubota, and Gou Young Koh
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Published April 1, 2026 - More info
J Clin Invest. 2026;136(7):e205881. https://doi.org/10.1172/JCI205881.
© 2026 Lee et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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Abstract
Emerging evidence indicates that angiopoietin-2 (Angpt2), a well-recognized vascular destabilizing factor, is a biomarker of poor outcome in ischemic heart disease. However, its precise role in postischemic cardiovascular remodeling is poorly understood. Here, we show that Angpt2 plays multifaceted roles in the exacerbation of cardiac hypoxia and inflammation after myocardial ischemia. Angpt2 was highly expressed in endothelial cells at the infarct border zone after myocardial infarction (MI) or ischemia/reperfusion injury in mice. In the acute phase of MI, endothelial-derived Angpt2 antagonized Angpt1/Tie2 signaling, which was greatly involved in pericyte detachment, vascular leakage, increased adhesion molecular expression, degradation of the glycocalyx and extracellular matrix, and enhanced neutrophil infiltration and hypoxia in the infarct border area. In the chronic remodeling phase after MI, endothelial- and macrophage-derived Angpt2 continuously promoted abnormal vascular remodeling and proinflammatory macrophage polarization through integrin α5β1 signaling, worsening cardiac hypoxia and inflammation. Accordingly, inhibition of Angpt2 either by gene deletion or using an anti-Angpt2 blocking antibody substantially alleviated these pathological findings and ameliorated postischemic cardiovascular remodeling. Blockade of Angpt2 thus has potential as a therapeutic option for ischemic heart failure.
Authors
Seung-Jun Lee, Choong-kun Lee, Seok Kang, Intae Park, Yoo Hyung Kim, Seo Ki Kim, Seon Pyo Hong, Hosung Bae, Yulong He, Yoshiaki Kubota, Gou Young Koh
Original citation: J Clin Invest. 2018;128(11):5018–5033. https://doi.org/10.1172/JCI99659
Citation for this corrigendum: J Clin Invest. 2026;136(7):e205881. https://doi.org/10.1172/JCI205881
The authors recently became aware of the following errors in the original manuscript: In Figure 7K, the ATN-161 image was incorrect and was derived from the same sample as the Figure 7H WT image; in Supplemental Figure 6B, the WT TER119/NG2/CD31 image was incorrect and was derived from the same sample as the Supplemental 6B Tie2iΔEC TER119/NG2/CD31 image; in Supplemental Figure 8B, the MI 3d images were incorrect and were derived from the same samples as Figure 6E Angpt2iΔEC; in Supplemental Figure 11A, the Sham ZO1/CD31 image was incorrect and was derived from the same sample as Figure 9D Sham FITC-Lectin/CD31; and in Supplemental Figure 13A, the I/R 7d Angpt2/CD31 image was incorrect and was derived from the same sample as shown in Figure 3F. The authors confirmed that the quantitative data accompanying these errors were obtained independently and were unaffected by the corrections. The legend for Supplemental Figure 8B was also updated for clarity and accuracy. The corrected figures, based on the original source data, are provided below and in the updated supplemental materials. The HTML and PDF versions of the paper have been updated.
Figure 7Angpt2/integrin α5β1 signaling is positively associated with pERK expression in macrophages in ischemic heart.
The authors regret the errors.
Copyright © 2026 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)