Key result
IL-11 inhibition protects against cardiac fibrosis and preserves function in rodent models.
Why the study?
IL-11 is an important cytokine in cardiac fibrosis, but its role and therapeutic potential in this process remain little explored with many questions persisting.
Does IL-11 modulation affect cardiac fibrosis and function in rodent models?
Systematic Review (n=8)
Does IL-11 modulation affect cardiac fibrosis and function in rodent models?
In rodent models, IL-11 overexpression induces cardiac fibrosis while its inhibition is protective, suggesting IL-11 as a promising therapeutic target for heart failure.
IL-11 inhibition may merit antifibrotic testing in heart failure; animal data leave open clinical translation.
Fibrosis is one of the main factors that impair the function of many organs. In the heart, fibrosis leads to contractile dysfunction and arrhythmias, which are important in the development of heart failure. Interleukin (IL)-11 is regulated in various heart diseases and has recently been reported to be an important cytokine in fibrosis in this organ. However, this topic has been little explored, and many questions persist. Thus, this systematic review aimed to report on possible IL-11 therapies evaluated in rodent model-induced cardiac fibrosis. Inclusion criteria were experimental in vivo studies that used different rodent models for cardiac fibrosis associated with IL-11 interventions, without year and language restrictions. The search in PubMed, Web of Science, and Embase databases was performed in October 2022. The risk of bias assessment of the studies was based on the guidelines of the SYRCLE tool, and data from the selected articles were also presented in a table as a narrative description. This review was based on eight studies in which five different interventions were used: recombinant human IL-11 (rhIL-11), anti-IL11 (X203), recombinant mouse IL-11 (rmIL-11), lentivirus (LV)-IL-11 + lutein, and anti-IL11RA (X209). Based on the included studies, the results were variable, with IL-11 overexpression inducing cardiac fibrosis, while inhibition protected against this process, preserving the function of this organ. Therefore, IL-11 stands out as a promising therapeutic target for cardiac fibrosis. However, further studies are needed to understand the mechanisms triggered by each treatment, as well as its safety and immunogenicity.
No takes yet. Share an insight, caveat, or question.
Braga et al. (2024) conducted a systematic review in Cardiac fibrosis (n=8). IL-11 interventions (rhIL-11, rmIL-11, anti-IL11, anti-IL11RA, LV-IL-11) vs. Untreated controls was evaluated on Cardiac fibrosis. IL-11 overexpression induced cardiac fibrosis, while its inhibition protected against this process and preserved cardiac function in rodent models.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: