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Correction to Int. J. Mol. Sci. 2022, 23(24), 16166.
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Correction

Correction: Yin et al. Angiogenesis–Browning Interplay Mediated by Asprosin-Deficiency Contributes to Weight Loss in Mice with Obesity. Int. J. Mol. Sci. 2022, 23, 16166

by
Tingting Yin
1,2,
Sheng Chen
1,2,
Guohua Zeng
1,2,
Wanwan Yuan
1,2,
Yanli Lu
1,2,
Yanan Zhang
1,2,
Qianqian Huang
1,2,
Xiaowei Xiong
1,2,
Baohua Xu
3,* and
Qiren Huang
1,2,*
1
Key Provincial Laboratory of Basic Pharmacology, Nanchang University, Nanchang 330006, China
2
Department of Pharmacology, School of Pharmacy, Nanchang University, Nanchang 330006, China
3
Jiangxi Province Key Laboratory of Laboratory Animal, Nanchang 330006, China
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2025, 26(6), 2499; https://doi.org/10.3390/ijms26062499
Submission received: 4 December 2024 / Accepted: 30 January 2025 / Published: 11 March 2025
(This article belongs to the Section Molecular Endocrinology and Metabolism)
Browse Figures
Versions Notes
In the original publication [1], “asprosin-knockout” is somewhat inappropriate, but we indeed generated ASP deficiency in adipose tissue of mice, evidenced by the attachment titled “Supplementary Materials”. Therefore, “Asprosin-Knockout”, “ASP-knockout”, “ASP-CKO”, and “ASP−/−” in the original publication [1] were revised to “Asprosin-Deficiency”, “ASP-deficiency”, “ASP-deficiency”, and “ASP-def” throughout the paper, including the corresponding Figures 1–4. The authors state that the scientific conclusions are unaffected. This correction was approved by the academic editor. The original publication has also been updated.
The correct Figure 1 and Figure 2 appear below.

Reference

  1. Yin, T.; Chen, S.; Zeng, G.; Yuan, W.; Lu, Y.; Zhang, Y.; Huang, Q.; Xiong, X.; Xu, B.; Huang, Q. Angiogenesis–browning interplay mediated by asprosin-deficiency contributes to weight loss in mice with obesity. Int. J. Mol. Sci. 2022, 23, 16166. [Google Scholar] [CrossRef] [PubMed]
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Figure 1. ASP-deficiency alleviates mouse obesity induced by HFD. Representative photographs (A) of C57 BL/6 mice. Body weight (B), length (C), and Lee’s index (D) were measured and calculated. Representative photographs (E) and weights (F) from eWAT in mice. Representative HE-staining images from eWAT (E) and average diameters of adipocytes from eWAT. (G) Data are presented as means ± SEM from 3 independent experiments (n = 3). Two-way ANOVAs were performed, followed by unpaired two-tailed Student’s t-tests. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. WT-ND group; # p < 0.05, ## p < 0.01 vs. WT-HFD group; & p < 0.05, && p < 0.01 vs. ASP-def-ND group; ns = no significance. WT-ND: wild-type mice fed with normal diet; WT-HFD: wild-type mice fed with high-fat diet; ASP-def-ND: ASP-deficient mice fed with normal diet; ASP-def-HFD: ASP-deficient mice fed with high-fat diet; eWAT: epididymal white adipose tissue. Scale bars in the images of HE staining in (E) 20 µm. ASP: asprosin, HE staining: hematoxylin–eosin staining.
Figure 1. ASP-deficiency alleviates mouse obesity induced by HFD. Representative photographs (A) of C57 BL/6 mice. Body weight (B), length (C), and Lee’s index (D) were measured and calculated. Representative photographs (E) and weights (F) from eWAT in mice. Representative HE-staining images from eWAT (E) and average diameters of adipocytes from eWAT. (G) Data are presented as means ± SEM from 3 independent experiments (n = 3). Two-way ANOVAs were performed, followed by unpaired two-tailed Student’s t-tests. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. WT-ND group; # p < 0.05, ## p < 0.01 vs. WT-HFD group; & p < 0.05, && p < 0.01 vs. ASP-def-ND group; ns = no significance. WT-ND: wild-type mice fed with normal diet; WT-HFD: wild-type mice fed with high-fat diet; ASP-def-ND: ASP-deficient mice fed with normal diet; ASP-def-HFD: ASP-deficient mice fed with high-fat diet; eWAT: epididymal white adipose tissue. Scale bars in the images of HE staining in (E) 20 µm. ASP: asprosin, HE staining: hematoxylin–eosin staining.
Ijms 26 02499 g001
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Figure 2. ASP-deficiency promotes angiogenesis and browning of white adipose in vivo. Representative images (A) of immunohistochemistry and immunofluorescence. Relative expression levels in situ of UCP1 (B) and CD31 (C) in eWAT normalized by adipocyte size. Expression levels of CD31 in eWAT by Western blot (D,E). Expression levels of the browning-related proteins, including PRDM16, PGC-1α, and UCP-1, in eWAT (F,G). Data are presented as means ± SEM from three independent experiments (n = 3). Two-way ANOVAs were performed followed by unpaired two-tailed Student’s t-tests. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. the WT-ND group; # p < 0.05, ## p < 0.01 vs. the WT-HFD group; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. the ASP-def-ND group. WT-ND: wild-type mice fed with normal diet; WT-HFD: wild-type mice fed with high-fat diet; ASP-def-ND: ASP-deficient mice fed with normal diet; ASP-def-HFD: ASP-deficient mice fed with high-fat diet; eWAT: epididymal white adipose tissue. Scale bars in (A) 20 μm. ASP: asprosin, UCP1: uncoupling protein 1, PGC1-α: PPARgamma coactivator 1, PRDM16: PRD1-BF-1-RIZ1 homologous domain-containing protein 16.
Figure 2. ASP-deficiency promotes angiogenesis and browning of white adipose in vivo. Representative images (A) of immunohistochemistry and immunofluorescence. Relative expression levels in situ of UCP1 (B) and CD31 (C) in eWAT normalized by adipocyte size. Expression levels of CD31 in eWAT by Western blot (D,E). Expression levels of the browning-related proteins, including PRDM16, PGC-1α, and UCP-1, in eWAT (F,G). Data are presented as means ± SEM from three independent experiments (n = 3). Two-way ANOVAs were performed followed by unpaired two-tailed Student’s t-tests. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. the WT-ND group; # p < 0.05, ## p < 0.01 vs. the WT-HFD group; & p < 0.05, && p < 0.01, &&& p < 0.001 vs. the ASP-def-ND group. WT-ND: wild-type mice fed with normal diet; WT-HFD: wild-type mice fed with high-fat diet; ASP-def-ND: ASP-deficient mice fed with normal diet; ASP-def-HFD: ASP-deficient mice fed with high-fat diet; eWAT: epididymal white adipose tissue. Scale bars in (A) 20 μm. ASP: asprosin, UCP1: uncoupling protein 1, PGC1-α: PPARgamma coactivator 1, PRDM16: PRD1-BF-1-RIZ1 homologous domain-containing protein 16.
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MDPI and ACS Style

Yin, T.; Chen, S.; Zeng, G.; Yuan, W.; Lu, Y.; Zhang, Y.; Huang, Q.; Xiong, X.; Xu, B.; Huang, Q. Correction: Yin et al. Angiogenesis–Browning Interplay Mediated by Asprosin-Deficiency Contributes to Weight Loss in Mice with Obesity. Int. J. Mol. Sci. 2022, 23, 16166. Int. J. Mol. Sci. 2025, 26, 2499. https://doi.org/10.3390/ijms26062499

AMA Style

Yin T, Chen S, Zeng G, Yuan W, Lu Y, Zhang Y, Huang Q, Xiong X, Xu B, Huang Q. Correction: Yin et al. Angiogenesis–Browning Interplay Mediated by Asprosin-Deficiency Contributes to Weight Loss in Mice with Obesity. Int. J. Mol. Sci. 2022, 23, 16166. International Journal of Molecular Sciences. 2025; 26(6):2499. https://doi.org/10.3390/ijms26062499

Chicago/Turabian Style

Yin, Tingting, Sheng Chen, Guohua Zeng, Wanwan Yuan, Yanli Lu, Yanan Zhang, Qianqian Huang, Xiaowei Xiong, Baohua Xu, and Qiren Huang. 2025. "Correction: Yin et al. Angiogenesis–Browning Interplay Mediated by Asprosin-Deficiency Contributes to Weight Loss in Mice with Obesity. Int. J. Mol. Sci. 2022, 23, 16166" International Journal of Molecular Sciences 26, no. 6: 2499. https://doi.org/10.3390/ijms26062499

APA Style

Yin, T., Chen, S., Zeng, G., Yuan, W., Lu, Y., Zhang, Y., Huang, Q., Xiong, X., Xu, B., & Huang, Q. (2025). Correction: Yin et al. Angiogenesis–Browning Interplay Mediated by Asprosin-Deficiency Contributes to Weight Loss in Mice with Obesity. Int. J. Mol. Sci. 2022, 23, 16166. International Journal of Molecular Sciences, 26(6), 2499. https://doi.org/10.3390/ijms26062499

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