Aldosterone-induced inflammatory response of mesangial cells via angiotension II receptors

Hao, Jianbing; Ren, Liwei; Zhang, Lei; Kong, Deyang; Hao, Lirong

doi:10.1177/1470320313519486

Cited by 5 publications

(3 citation statements)

References 26 publications

(31 reference statements)

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“…Aldosterone is involved in the inflammation of various tissues [5,6]. Our previous study also successively confirmed that aldosterone contributes to inflammation of different tissues involved in CKD such as the heart, kidney, and peritoneum [7]. This suggests that aldosterone is a significant cause of chronic inflammation.…”

Section: Introductionsupporting

confidence: 72%

The Crosstalk between Calcium Ions and Aldosterone Contributes to Inflammation, Apoptosis, and Calcification of VSMC via the AIF-1/NF-κB Pathway in Uremia

Hao

Jie

Zhang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Vascular calcification is a major complication of maintenance hemodialysis patients. Studies have confirmed that calcification mainly occurs in the vascular smooth muscle cells (VSMC) of the vascular media. However, the exact pathogenesis of VSMC calcification is still unknown. This study shows that the crosstalk between calcium and aldosterone via the allograft inflammatory factor 1 (AIF-1) pathway contributes to calcium homeostasis and VSMC calcification, which is a novel mechanism of vascular calcification in uremia. In vivo results showed that the level of aldosterone and inflammatory factors increased in calcified arteries, whereas no significant changes were observed in peripheral blood. However, the expression of inflammatory factors markedly increased in the peripheral blood of uremic rats without aortic calcification and gradually returned to normal levels with aggravation of aortic calcification. In vitro results showed that there was an interaction between calcium ions and aldosterone in macrophages or VSMC. Calcium induced aldosterone synthesis, and in turn, aldosterone also triggered intracellular calcium content upregulation in macrophages or VSMC. Furthermore, activated macrophages induced inflammation, apoptosis, and calcification of VSMC. Activated VSMC also imparted a similar effect on untreated VSMC. Finally, AIF-1 enhanced aldosterone- or calcium-induced VSMC calcification, and NF-κB inhibitors inhibited the effect of AIF-1 on VSMC. These in vivo and in vitro results suggest that the crosstalk between calcium ions and aldosterone plays an important role in VSMC calcification in uremia via the AIF-1/NF-κB pathway. Local calcified VSMC induced the same pathological process in surrounding VSMC, thereby contributing to calcium homeostasis and accelerating vascular calcification.

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Section: Introductionsupporting

confidence: 72%

The Crosstalk between Calcium Ions and Aldosterone Contributes to Inflammation, Apoptosis, and Calcification of VSMC via the AIF-1/NF-κB Pathway in Uremia

Hao

Jie

Zhang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…However, the relationship between MDH2 and glycolysis remained unknown. Glycolysis is one of the classic pathways through which cells metabolize acetyl CoA, which was essential for maintaining TCA cycle activity [ 17 ]. Moreover, high levels of acetyl CoA promoted histone acetylation, putting cells into a proanabolic state, thereby promoting cell growth [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

MDH1 and MDH2 Promote Cell Viability of Primary AT2 Cells by Increasing Glucose Uptake

Yang

et al. 2022

Computational and Mathematical Methods in Medicine

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Background. Acute lung injury (ALI) is a clinical disease with high morbidity and mortality, with limited treatment means. For primary alveolar epithelial type II (AT2) cells, glycolysis is an essential bioenergetic process. However, the significance of AT2 cell glycolysis in sepsis ALI remains unknown. Methods and Results. In the current study, based on microarray analysis, real-time quantitative PCR, and Western blotting, we found that the hsa00020: citrate cycle pathway was inactivated, specifically its downstream gene: malate dehydrogenase 1 (MDH1) and MDH2 in ALI. In this context, lipopolysaccharides (LPS) were used to construct the septic-ALI mouse model and the biological function of MDH1 and MDH2 in primary alveolar epithelial type II (AT2) cells was explored. Through CCK-8, EdU, transwell, and apoptosis assays, we found that MDH1 and MDH2 promoted the cell vitality of AT2 cells, which relied on MDH1 and MDH2 to promote the glucose intake of AT2 cells. Conclusion. Overall, these findings suggest that targeting MDH1/MDH2-mediated AT2 cell glycolysis may be a potential strategy for ALI patients.

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“…Moreover, advanced glycation end products (AGEs) or dipeptidyl peptidase-4 (DPP-4) can induce the up-regulation of NF-κB p65 or CCL2 mRNA levels in tubular cells [28]. Aldosterone can induce an inflammatory response through the activation of NF-κB and CCL2 in mesangial cells under the high glucose condition via the angiotensin II receptors pathways [29]. High glucose can induce the phosphorylation and sumoylation of IKKγ and activated NF-κB signaling, accompanied by up-regulated CCL2 and IL-6 [30].…”

Section: The Potential Role Of Ccl2 In Diabetic Nephropathymentioning

confidence: 99%

The Role of Chemokines and Chemokine Receptors in Diabetic Nephropathy

Chang¹,

Chen

2020

IJMS

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Kidney function decline is one of the complications of diabetes mellitus and may be indicated as diabetic nephropathy (DN). DN is a chronic inflammatory disease featuring proteinuria and a decreasing glomerular filtration rate. Despite several therapeutic options being currently available, DN is still the major cause of end-stage renal disease. Accordingly, widespread innovation is needed to improve outcomes in patients with DN. Chemokines and their receptors are critically involved in the inflammatory progression in the development of DN. Although recent studies have shown multiple pathways related to the chemokine system, the specific and direct effects of chemokines and their receptors remain unclear. In this review, we provide an overview of the potential role and mechanism of chemokine systems in DN proposed in recent years. Chemokine system-related mechanisms may provide potential therapeutic targets in DN.

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Aldosterone-induced inflammatory response of mesangial cells via angiotension II receptors

Cited by 5 publications

References 26 publications

The Crosstalk between Calcium Ions and Aldosterone Contributes to Inflammation, Apoptosis, and Calcification of VSMC via the AIF-1/NF-κB Pathway in Uremia

The Crosstalk between Calcium Ions and Aldosterone Contributes to Inflammation, Apoptosis, and Calcification of VSMC via the AIF-1/NF-κB Pathway in Uremia

MDH1 and MDH2 Promote Cell Viability of Primary AT2 Cells by Increasing Glucose Uptake

The Role of Chemokines and Chemokine Receptors in Diabetic Nephropathy

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