Mesenchymal Stem Cell Therapy in Diabetic Cardiomyopathy

Cells

Rosália Mendez-Otero¹  Renata G. J. Gonçalves¹  Juliana F. Vasques²  Mauro P. L. de Sá³  Jaqueline S. da Silva⁴  Bruna S. Rocha⁴  Bianca Nascimento-Carlos⁴  Gisele Zapata-Sudo⁴  Tadeu L. Montagnoli⁴ 

[1] Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, Rio de Janeiro 21941-170, RJ, Brazil;Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, Rio de Janeiro 21941-170, RJ, Brazil;Instituto do Coração Edson Saad, Faculdade de Medicina, Universidade Federal do Rio de Janeiro, Street Prof. Rodolpho Paulo Rocco, 255, Rio de Janeiro 21941-617, RJ, Brazil;Programa de Pesquisa em Desenvolvimento de Fármacos, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho, 373, Rio de Janeiro 21941-902, RJ, Brazil;

关键词: diabetes mellitus;    cardiac remodeling;    diabetic cardiomyopathy;    mesenchymal stromal cells;    pro-inflammatory cytokines;    oxidative stress;   

DOI  :  10.3390/cells11020240

来源: DOAJ

【 摘 要 】

The incidence and prevalence of diabetes mellitus (DM) are increasing worldwide, and the resulting cardiac complications are the leading cause of death. Among these complications is diabetes-induced cardiomyopathy (DCM), which is the consequence of a pro-inflammatory condition, oxidative stress and fibrosis caused by hyperglycemia. Cardiac remodeling will lead to an imbalance in cell survival and death, which can promote cardiac dysfunction. Since the conventional treatment of DM generally does not address the prevention of cardiac remodeling, it is important to develop new alternatives for the treatment of cardiovascular complications induced by DM. Thus, therapy with mesenchymal stem cells has been shown to be a promising approach for the prevention of DCM because of their anti-apoptotic, anti-fibrotic and anti-inflammatory effects, which could improve cardiac function in patients with DM.

【 授权许可】

Unknown