The Influence of IL-11 on Cardiac Fibrosis in Experimental Models: A Systematic Review

Author:

Braga Yarlla Loyane Lira1,do Carmo Neto José Rodrigues1,Franco Pablo Igor Ribeiro1ORCID,Helmo Fernanda Rodrigues2,dos Reis Marlene Antônia2,de Oliveira Flávia Aparecida1,Celes Mara Rúbia Nunes1ORCID,da Silva Marcos Vinícius3ORCID,Machado Juliana Reis124

Affiliation:

1. Department of Bioscience and Technology, Institute of Tropical Pathology and Public Health, Federal University of Goias, Goiania 74605-450, GO, Brazil

2. General Pathology, Federal University of Triângulo Mineiro, Uberaba 38025-180, MG, Brazil

3. Department of Microbiology, Immunology and Parasitology, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba 38025-180, MG, Brazil

4. Department of General Pathology, Federal University of Triângulo Mineiro, Uberaba 38025-180, MG, Brazil

Abstract

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.

Funder

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Publisher

MDPI AG

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