GSK3β has been known to dictate the activity of MAPK kinases39,40,41, including p38, ERK and JNK, which have been implicated in renal inflammation and fibrogenesis in progressive AKI38.
EPHA3 is recurrently mutated in adenocarcinoma [62], [63] and has been implicated in renal carcinoma, glioblastoma, colorectal, breast and lung cancer [63], [64], [65], [66], [67].
Several components of the NLRP3 inflammasome have been implicated in renal disease (Table 2).
Both downstream effectors of Ras, ERK1/2, and Akt have been implicated in renal damage response in obstructive nephropathy.
VEGF-mediated permeability has also been implicated in renal failure, arthritis, psoriasis, and coronary disease, but their consideration is beyond the scope of this review.
In light of these findings, it is perhaps not surprising that LPA has been implicated in renal (Pradere et al., 2007), hepatic (Watanabe et al., 2007a, b) and pulmonary fibrosis (Tager et al., 2008; Xu et al., 2009).
Several E. coli virulence factors, including toxins, are implicated in renal inflammatory injury and bacteremia, but the mechanisms of translocation from the renal system to the bloodstream is poorly understood.
Imbalance in glucose and lipid metabolism of POKO mice compared with ob/ob mice showed an incipient insulin resistance associated with decreased adiponectin expression in kidney, a mechanism that could be implicated in renal failure induced by glucolipotoxicity.
Imbalance in the glucose metabolism of the POKO mice compared with ob/ob mice shows an incipient insulin resistance in kidney, a mechanism that could be implicated in renal failure induced by glucolipotoxicity.
The findings of this study let us hypothesize that TCTP is involved in renal tubular functions, since tubular cells express the protein at the highest level, and that it might be implicated in renal carcinogenesis since it is expressed in all the histotypes of renal cell carcinoma and not in benign tumors.
Recent studies have shown that reactive oxygen species (ROS), inflammatory mediators such as intracellular adhesion molecule (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) [ 7, 8] as well as infiltration of inflammatory cells are implicated in renal ischemia reperfusion injury [ 2].
