Corrigendum
Open Access | 
10.1172/jci.insight.205164
Corrigendum to: Bmal1 is involved in the regulation of macrophage cholesterol homeostasis
Xiaoyue Pan, John O’Hare, Cyrus Mowdawalla, Samantha Mota, Nan Wang, and M. Mahmood Hussain
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Published May 5, 2026 - More info
JCI Insight. 2026;11(5):e205164. https://doi.org/10.1172/jci.insight.205164.
© 2026 Pan 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
Atherosclerotic cardiovascular disease is a major contributor to the global disease burden. We previously demonstrated that Clock-mutant mice, and mice with global or liver-specific Bmal1 deficiency, exhibit enhanced atherosclerosis because of overproduction of lipoproteins and sustained hyperlipidemia. Atherosclerosis initiation depends on cholesterol accumulation in subendothelial macrophages (Mφs). To clarify the role of Bmal1 in Mφ function and atherosclerosis, we used several global and myeloid-specific Bmal1-deficient mouse models. Mφ-specific Bmal1-deficient mice had similar plasma lipid levels, higher Mφ cholesterol content, and displayed greater atherosclerosis compared with controls. We attempted to understand molecular mechanisms for increased cellular cholesterol levels. Bmal1-deficient Mφs exhibited: (a) elevated expression of Cd36 and uptake of oxLDL; (b) diminished expression of Abca1 and Abcg1, and decreased cholesterol efflux and reverse cholesterol transport; and (c) reduced Npc1 and Npc2 expression and diminished cholesterol egress from lysosomes. Molecular studies revealed that Bmal1 directly regulates basal and cyclic expression of Npc1 and Npc2 by binding the E-box motif (CANNTG) sequence recognized by Bmal1 in their promoters and indirectly regulates the basal and temporal regulation of Cd36 and Abca1/Abcg1 involving Rev-erbα and Znf202 repressors, respectively. In conclusion, Mφ Bmal1 is a key regulator of the uptake of modified lipoproteins, cholesterol efflux, lysosomal cholesterol egress, and atherosclerosis and, therefore, may be a master regulator of cholesterol metabolism in Mφs. Restoration of Mφ Bmal1 expression or blocking of factors that decrease its activity may be effective in preventing atherosclerosis.
Authors
Xiaoyue Pan, John O’Hare, Cyrus Mowdawalla, Samantha Mota, Nan Wang, M. Mahmood Hussain
Original citation: JCI Insight. 2025;10(21):e194304. https://doi.org/10.1172/jci.insight.194304
Citation for this corrigendum: JCI Insight. 2026;11(5):e205164. https://doi.org/10.1172/jci.insight.205164
During final revision of the manuscript, several text changes and 3 references were inadvertently omitted. The HTML and PDF versions have been updated online. The Journal has also published an online version of the article that highlights the changes that have been made (Supplemental File, Marked).
The authors and the Journal regret the error.
