Abstract:Uterine sensitization-associated gene-1 (USAG-1), originally identified as a secretory protein preferentially expressed in the sensitized rat endometrium, has been determined to modulate bone morphogenetic protein (BMP) and Wnt expression to play important roles in kidney disease. USAG-1 affects the progression of acute and chronic kidney damage and the recovery of allograft kidney function by regulating the BMP and Wnt signaling pathways. Moreover, USAG-1 has been found to be involved in the process of T cell… Show more
“…Many BMP antagonists have been linked to kidney disease states. 36 In fact, GREM2 overexpression increases apoptosis in cultured human podocytes. 37 Figure 6 Expression of selected genes downstream of the BMP antagonist GREM2 (A–J) RT-qPCR was used to generate data for all Jerboa samples (n = 42).…”
“…Many BMP antagonists have been linked to kidney disease states. 36 In fact, GREM2 overexpression increases apoptosis in cultured human podocytes. 37 Figure 6 Expression of selected genes downstream of the BMP antagonist GREM2 (A–J) RT-qPCR was used to generate data for all Jerboa samples (n = 42).…”
“…It is highly expressed as a cancer suppressor in the kidney ( Blish et al, 2009 ). Recent study show that USAG-1 protecting renal tubules from interstitial fibrosis caused by ischemia-reperfusion injury or drug toxicity injury by regulating the Wnt signal and other related pathways ( Tanaka et al, 2008 ; Lu et al, 2019 ; Badshah et al, 2019 ; Blish,et al, 2009 ; Li et al, 2021 ).…”
Section: Wnt Signaling Pathway and Renal Fibrosismentioning
confidence: 99%
“…It has been demonstrated that exogenous Wnt1 prevents acute kidney injury and subsequent chronic renal injury ( Hong et al, 2021 ). Supplement of the reduced Wnt signal and neutralizing abnormal Wnt cascade activation may be potential strategies for therapeutic intervention of progressive renal diseases ( von Toerne, et al, 2009 ; Luo et al, 2007 ; He et al, 2009 ; Li, et al, 2021 ). However, the involvement of Wnt Non-canonical pathway with DN progression had not been paid enough attention in details.…”
Diabetic nephropathy (DN) is a serious kidney-related complication of both type 1 and type 2 diabetes mellitus (T1DM, T2DM) and the second major cause of end-stage kidney disease. DN can lead to hypertension, edema, and proteinuria. In some cases, DN can even progress to kidney failure, a life-threatening condition. The precise etiology and pathogenesis of DN remain unknown, although multiple factors are believed to be involved. The main pathological manifestations of DN include mesangial expansion, thickening of the glomerular basement membrane, and podocyte injury. Eventually, these pathological manifestations will lead to glomerulosclerosis, thus affecting renal function. There is an urgent need to develop new strategies for the prevention and treatment of DN. Existing evidence shows that the Wnt signaling cascade plays a key role in regulating the development of DN. Previous studies focused on the role of the Wnt canonical signaling pathway in DN. Subsequently, accumulated evidence on the mechanism of the Wnt non-canonical signaling indicated that Wnt/Ca2+ and Wnt/PCP also have essential roles in the progression of DN. In this review, we summarize the specific mechanisms of Wnt signaling in the occurrence and development of DN in podocyte injury, mesangial cell injury, and renal fibrosis. Also, to elucidate the significance of the Wnt canonical pathway in the process of DN, we uncovered evidence supporting that both Wnt/PCP and Wnt/Ca2+ signaling are critical for DN development.
“…The restoration of Sostdc1 signalling may suggest a novel strategy for treating renal clear cell carcinoma (Blish et al, 2008). However, interestingly, a previous systematic review concluded that Sostdc1 inhibits the progression of kidney-related cancers but promotes some kidney diseases (Li et al, 2021), including acute and chronic renal injuries (Tanaka et al, 2008), and renal fibrosis (Hamasaki et al, 2012).…”
Sclerostin domain-containing protein-1 (Sostdc1) is a member of the sclerostin family and encodes a secreted 28–32 kDa protein with a cystine knot-like domain and two N-linked glycosylation sites. Sostdc1 functions as an antagonist to bone morphogenetic protein (BMP), mediating BMP signaling. It also interacts with LRP6, mediating LRP6 and Wnt signaling, thus regulating cellular proliferation, differentiation, and programmed cell death. Sostdc1 plays various roles in the skin, intestines, brain, lungs, kidneys, and vasculature. Deletion of Sostdc1 gene in mice resulted in supernumerary teeth and improved the loss of renal function in Alport syndrome. In the skeletal system, Sostdc1 is essential for bone metabolism, bone density maintenance, and fracture healing. Recently, Sostdc1 has been found to be closely related to the development and progression of multiple cancer types, including breast, renal, gastric, and thyroid cancers. This article summarises the role of Sostdc1 in skeletal biology and related cancers to provide a theoretical basis for the treatment of related diseases.
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