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10.1073/pnas.1419901111

http://scihub22266oqcxt.onion/10.1073/pnas.1419901111
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C4273328!4273328!25422468
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suck abstract from ncbi


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pmid25422468      Proc+Natl+Acad+Sci+U+S+A 2014 ; 111 (50): E5420-8
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  • Overactive cannabinoid 1 receptor in podocytes drives type 2 diabetic nephropathy #MMPMID25422468
  • Jourdan T; Szanda G; Rosenberg AZ; Tam J; Earley BJ; Godlewski G; Cinar R; Liu Z; Liu J; Ju C; Pacher P; Kunos G
  • Proc Natl Acad Sci U S A 2014[Dec]; 111 (50): E5420-8 PMID25422468show ga
  • Diabetic nephropathy is the leading cause of chronic kidney disease in the United States, and one of the most significant long-term complications of both type 1 and type 2 diabetes, which currently lack fully effective therapy. Hyperglycemia and activation of the renin-angiotensin system (RAS) are thought to be the two main drivers of this pathology. We have recently shown that selective blockade of peripheral cannabinoid receptor-1 (CB1R) delayed and attenuated the development of type 2 diabetes in a rat model. Here we show that the nephropathy-inducing effects of both hyperglycemia and activation of the RAS involve CB1R activation in glomerular podocytes, and that antagonism of peripheral CB1R could represent a novel, effective, and rational approach to both prevent and reverse diabetic nephropathy.
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