P. Singh, L. Bahrami, A. Castillo and D. S. Majid, “TNFα Type 2 Receptor Mediates Renal Inflammatory Response to Chronic Angiotensin II Administration with High Salt Intake in Mice,” American Journal of Physiology—Renal Physiology, Vol. 304, No. 7, 2013, pp. F991-F999. doi:10.1152/ajprenal. 00525.2012

has been cited by the following article:

• TITLE: The Effects of Insulin Resistance and Inflammation on Renal Proximal Tubule Sodium Transport and Hypertension

  AUTHORS: Shoko Horita, Motonobu Nakamura, Masashi Suzuki, Hideomi Yamada, George Seki

  KEYWORDS: Insulin; Inflammation; TNF-α; Proximal Tubule; Insulin Resistance; PPARγ; Thiazolidinediones

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.3 No.5A, August 19, 2013

  ABSTRACT: Insulin resistance, closely linked to inflammation, is recognized as a key factor in the onset and aggravation of diabetes, cardio-renal syndrome, hypertension, and obesity. In the renal proximal tubule, insulin resistance may increase renal sodium reabsorption, leading to hypertension, edema and sometimes heart failure. Recently some anti-diabetic agents have been shown to have effects on the transporters in renal proximal tubule. Because renal proximal tubule mediates about 70% of sodium reabsorption, it is quite important to clarify the function of renal proximal tubule under insulin resistance and inflammation.