Mariane Dos Santos1, Priscila Tamar Poletti2, Patrícia Milhoransa1, Odirlei André Monticielo3, Francisco Veríssimo Veronese4. 1. Graduate Program in Medical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil; Division of Nephrology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil; Laboratory of Molecular Biology Applied to Nephrology, Experimental Research Center, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil. 2. Division of Nephrology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil; Laboratory of Molecular Biology Applied to Nephrology, Experimental Research Center, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil. 3. Division of Rheumatology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil. 4. Graduate Program in Medical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil; Division of Nephrology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil; Laboratory of Molecular Biology Applied to Nephrology, Experimental Research Center, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil. Electronic address: fveronese@hcpa.edu.br.
Abstract
OBJECTIVES: Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease with renal involvement in over half of the cases. In lupus nephritis (LN), podocytes are injured at the structural and molecular level. Spontaneous or induced animal models of SLE can reproduce the glomerular damage, similar to what is observed in humans. In this review, murine models focusing the podocyte injury were summarized, and therapeutic strategies to protect the podocyte cell were explored. METHODS: Using the PubMed and MEDLINE databases from 1950 to 2015, literature search was conducted by article title and abstract, combining the following key words: "systemic lupus erythematosus," "lupus nephritis," "animal model," "podocyte injury," and "treatment." RESULTS: Published or in-press eligible studies that were published as full-length articles in English-language journals were considered. Articles were summarized according to podocyte structure and function, the podocyte injury resulting from spontaneous (NZB/W F1 hybrid, MRL/lpr, and BXSB-Yaa mice) or induced (chronic graft-versus-host disease and pristane) mice models of LN, and the protective effects of drug treatments on podocyte cell structure and function reported in these models. CONCLUSIONS: Murine models of SLE have proven useful for better comprehension of the multiple mechanisms involved in systemic autoimmunity that leads to LN. These critical tools should be considered when target therapies are designed to control this disorder.
OBJECTIVES: Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease with renal involvement in over half of the cases. In lupus nephritis (LN), podocytes are injured at the structural and molecular level. Spontaneous or induced animal models of SLE can reproduce the glomerular damage, similar to what is observed in humans. In this review, murine models focusing the podocyte injury were summarized, and therapeutic strategies to protect the podocyte cell were explored. METHODS: Using the PubMed and MEDLINE databases from 1950 to 2015, literature search was conducted by article title and abstract, combining the following key words: "systemic lupus erythematosus," "lupus nephritis," "animal model," "podocyte injury," and "treatment." RESULTS: Published or in-press eligible studies that were published as full-length articles in English-language journals were considered. Articles were summarized according to podocyte structure and function, the podocyte injury resulting from spontaneous (NZB/W F1 hybrid, MRL/lpr, and BXSB-Yaa mice) or induced (chronic graft-versus-host disease and pristane) mice models of LN, and the protective effects of drug treatments on podocyte cell structure and function reported in these models. CONCLUSIONS:Murine models of SLE have proven useful for better comprehension of the multiple mechanisms involved in systemic autoimmunity that leads to LN. These critical tools should be considered when target therapies are designed to control this disorder.