The impact of obesity in renal fibrosis

The World Health Organization (WHO) describes overweight and obesity as an atypical or excessive fataccumulation, usually classified by the BMI (Body Mass Index). Overweight and obesity can result in cardiovascular diseases, diabetes, cancer and also CKD in adults of both sexes and in adolescentes, among others (1). Na high BMI has been described as a major risk factor for CKD onset, because excessive fat levels promote renal dysfunction and hemodynamic alterations (1). Many studies have shown a close relationship between metabolic changes, dysfunctional alteration and expansion of adipose tissue and kidney injury. Na abnormal tissue repair, as in CKD, and a change in the normal pattern of adipokines production, as in obesity, can lead to na abnormal inflammatory cell’s recruitment, fibroblastos activation and extracelular matrix prodution which triggers the development of inflammation, oxidative stress and fibrosis (2). Unfortunately, the exact mechanism underlying the effect of obesity in renal fibrosis triggering and progression is still nuclear. The better understanding of the celular and molecular pathways involved in the crosstalk between obesity and renal inflammation and fibrosis are of major relevance for the development of novel biomarkers and therapeutic targets that will allow the enrichment of scientific eidence and the progression of more effective therapies. In this project, we aim to study the celular and molecular machanisms underlying obesity-related kidney fibrosis and the identification of potential therapeutic tagets for kidney disease