Key result
IL-5 deficiency promoted M2 macrophage differentiation and exacerbated cardiac remodeling and dysfunction by activating the STAT3 pathway in Angiotensin II-infused mice.
Why the study?
Interleukin-5 was reported to participate in cardiovascular diseases, prompting investigation into its effects on cardiac remodeling.
Does IL-5 deficiency exacerbate cardiac remodeling in Angiotensin II-infused mice?
Does IL-5 deficiency exacerbate cardiac remodeling in Angiotensin II-infused mice?
p-value: p=<0.05
IL-5 deficiency exacerbates cardiac remodeling and promotes M2 macrophage differentiation via the STAT3 pathway in Ang II-infused mice, suggesting IL-5 as a potential therapeutic target for preventing cardiac remodeling.
IL-5 deficiency effects in Ang II mice are hypothesis-generating; leaves open any role in human cardiac remodeling.
Interleukin-5 (IL-5) was reported to participate in cardiovascular diseases, this study aimed to investigate the effects of IL-5 on cardiac remodeling. Mice were infused with angiotensin II (Ang II), and we found cardiac IL-5 expression was time- and dose-dependently decreased after Ang II infusion, and was mainly derived from cardiac macrophages. Additionally, the effects of IL-5 knockout on Ang II-induced cardiac remodeling were observed, and the results exhibited that IL-5 deficiency significantly increased the expression of cardiac hypertrophy markers, elevated myocardial cell cross-sectional areas, and worsened cardiac dysfunction in Ang II-infused mice. IL-5 deletion also promoted M2 macrophage differentiation and exacerbated cardiac fibrosis. Effects of IL-5 on cardiac remodeling and M2 macrophage differentiation were reversed by S31-201. IL-5 knockout significantly increased the Ang II-induced mRNA expression of cardiac hypertrophy markers in myocardial cells that were co-cultured with macrophages, and this effect was also reversed by S31-201. Similar trends in the mRNA levels of fibrosis markers were observed when cardiac fibroblasts and macrophages were co-cultured. Our study suggests that IL-5 deficiency promotes M2 macrophages differentiation and exacerbating cardiac remodeling by activating the STAT3 pathway in Ang II-infused mice. IL-5 may be a potential target for the clinical prevention of cardiac remodeling.
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Shen et al. (2023) studied Cardiac remodeling. IL-5 knockout vs. Wild-type mice was evaluated on Cardiac remodeling and dysfunction (hypertrophy markers, fibrosis, and echocardiographic parameters) (p=<0.05). IL-5 deficiency promoted M2 macrophage differentiation and exacerbated cardiac remodeling and dysfunction by activating the STAT3 pathway in Angiotensin II-infused mice.
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