Effects of thromboxane prostanoid receptor deficiency on diabetic nephropathy induced by high fat diet and streptozotocin in mice

Cai, Juyu; Liu, Bin; Guo, Tingting; Zhang, Yingzhan; Wu, Xiangzhong; Leng, Jing; Zhu, Ningxia; Guo, Jinwei; Zhou, Yingbi

doi:10.1016/j.ejphar.2020.173254

Cited by 6 publications

(3 citation statements)

References 47 publications

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“…In addition, there are studies showing that in diabetic coronary arteries, the response to PGI 2 can be reversed from dilatation to contraction 53 . Consistent with these results, COX‐1 −/− (which removes endothelial PGI 2 synthesis under diabetic conditions), TP −/− , or EP3 −/− has been reported to improve diabetic complications, such as nephropathy, 51,110,111 although the causal relationship of such an effect with the improvement of endothelial dysfunction remains to be established.…”

Section: Vascular Pathologies and Therapeutic Implicationsmentioning

confidence: 71%

Endothelium‐dependent contraction: The non‐classical action of endothelial prostacyclin, its underlying mechanisms, and implications

Liu

Zhou

2021

The FASEB Journal

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Section: Vascular Pathologies and Therapeutic Implicationsmentioning

confidence: 71%

Endothelium‐dependent contraction: The non‐classical action of endothelial prostacyclin, its underlying mechanisms, and implications

Liu

Zhou

2021

The FASEB Journal

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“…Its expression can be induced by a number of inflammatory cytokines, mitogenic factors, and physical stimuli [29]. Previously, numerous studies revealed that COX-2 was increased in podocyte, glomerular mesangial cells, and renal tubular cells under HG condition, which contributed to the pathogenesis of DN [30][31][32][33]. Interestingly, the promoter region of the COX-2 gene contains several putative binding motifs for the binding of NF-κB [34].…”

Section: Discussionmentioning

confidence: 99%

PP2 Ameliorates Renal Fibrosis by Regulating the NF‐κB/COX‐2 and PPARγ/UCP2 Pathway in Diabetic Mice

Wei

Deng

Yang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Renal fibrosis is characterized by glomerulosclerosis and tubulointerstitial fibrosis in diabetic nephropathy (DN). We aimed to evaluate the effects of PP2 on renal fibrosis of DN. GSE33744 and GSE86300 were downloaded from the GEO database. Firstly, 839 DEGs were identified between nondiabetic and diabetic mice renal glomerular samples. COX-2 was selected to assess the effects of PP2 on renal glomerulosclerosis. In db/db mice, PP2 decreased the expression of COX-2, phosphorylated p65, and fibrotic proteins, accompanied with attenuated renal glomerulosclerosis. In cultured glomerular mesangial cells, high glucose- (HG-) induced p65 phosphorylation and COX-2 expression were attenuated by PP2 or NF-κB inhibitor PDTC. PP2, PDTC, or COX-2 inhibitor NS-398 ameliorated abnormal proliferation and expression of fibrotic proteins induced by HG. Secondly, 238 DEGs were identified between nondiabetic and diabetic mice renal cortex samples. UCP2 was selected to assess the effects of PP2 on renal tubulointerstitial fibrosis. In db/db mice, PP2 decreased the expression of PPARγ and UCP2, accompanied with attenuated renal tubulointerstitial fibrosis and EMT. In cultured proximal tubular cells, HG-induced PPARγ and UCP2 expression was inhibited by PP2 or PPARγ antagonist GW9662. PP2, GW9662, or UCP2 shRNA ameliorated HG-induced EMT. These results indicated that PP2 ameliorated renal fibrosis in diabetic mice.

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“…(41,42). In recent years, numerous studies have confirmed that COX-2 expression is significantly increased in mesangial cells, podocytes, and renal tubular epithelial cells induced by high glucose, as well as in the kidney of animal models of diabetes (43)(44)(45)(46)(47). Wei et al (43) pointed out that activation of the c-Src/NF-kB/COX-2 pathway in the high-glucose state promoted extracellular matrix accumulation and mesangial proliferation, which exacerbated glomerulosclerosis.…”

Section: Cyclooxygenase-2mentioning

confidence: 99%

Ferroptosis: a new strategy for Chinese herbal medicine treatment of diabetic nephropathy

Wei¹,

Liu²,

Tan³

et al. 2023

Front. Endocrinol.

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Diabetic nephropathy (DN) is a serious microvascular complication of diabetes. It has become a leading cause of death in patients with diabetes and end-stage renal disease. Ferroptosis is a newly discovered pattern of programmed cell death. Its main manifestation is the excessive accumulation of intracellular iron ion-dependent lipid peroxides. Recent studies have shown that ferroptosis is an important driving factor in the onset and development of DN. Ferroptosis is closely associated with renal intrinsic cell (including renal tubular epithelial cells, podocytes, and mesangial cells) damage in diabetes. Chinese herbal medicine is widely used in the treatment of DN, with a long history and definite curative effect. Accumulating evidence suggests that Chinese herbal medicine can modulate ferroptosis in renal intrinsic cells and show great potential for improving DN. In this review, we outline the key regulators and pathways of ferroptosis in DN and summarize the herbs, mainly monomers and extracts, that target the inhibition of ferroptosis.

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Effects of thromboxane prostanoid receptor deficiency on diabetic nephropathy induced by high fat diet and streptozotocin in mice

Cited by 6 publications

References 47 publications

Endothelium‐dependent contraction: The non‐classical action of endothelial prostacyclin, its underlying mechanisms, and implications

Endothelium‐dependent contraction: The non‐classical action of endothelial prostacyclin, its underlying mechanisms, and implications

PP2 Ameliorates Renal Fibrosis by Regulating the NF‐κB/COX‐2 and PPARγ/UCP2 Pathway in Diabetic Mice

Ferroptosis: a new strategy for Chinese herbal medicine treatment of diabetic nephropathy

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