Review Article - MCP-1: A Potential Target for Diabetic Microvascular Complications?

Yap, Hsiu Lye

doi:10.15406/unoaj.2017.05.00171

Cited by 3 publications

(3 citation statements)

References 27 publications

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“…These, in turn, are associated with increased expression of adhesion molecules and synthesis of pro-inflammatory cytokines, leading to hyperfiltration and glomerular lesions, typical of DKD. 75,76…”

Section: Introductionmentioning

confidence: 99%

Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation

Amorim¹,

Guedes²,

Vasconcelos³

et al. 2019

Arquivos Brasileiros De Cardiologia

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Chronic hyperglycemia is the key point of macro- and microvascular complications associated with diabetes mellitus. Excess glucose is responsible for inducing redox imbalance and both systemic and intrarenal inflammation, playing a critical role in the pathogenesis of diabetic kidney disease, which is currently the leading cause of dialysis in the world. The pathogenesis of the disease is complex, multifactorial and not fully elucidated; many factors and mechanisms are involved in the development, progression and clinical outcomes of the disease. Despite the disparate mechanisms involved in renal damage related to diabetes mellitus, the metabolic mechanisms involving oxidative/inflammatory pathways are widely accepted. The is clear evidence that a chronic hyperglycemic state triggers oxidative stress and inflammation mediated by altered metabolic pathways in a self-perpetuating cycle, promoting progression of cell injury and of end-stage renal disease. The present study presents an update on metabolic pathways that involve redox imbalance and inflammation induced by chronic exposure to hyperglycemia in the pathogenesis of diabetic kidney disease.

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Section: Introductionmentioning

confidence: 99%

Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation

Amorim¹,

Guedes²,

Vasconcelos³

et al. 2019

Arquivos Brasileiros De Cardiologia

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“…Previous studies reported that the levels of chemokines had significantly increased in patients with DR and the MCP‐1 was the most frequently added chemokine in serum and vitreous levels (Elner et al 1995; El‐Asrar et al 1997; Capeans et al 1998). It should be noted that the MCP‐1 plays a pivotal role in vascular inflammation through induction, activation, and recruitment of monocytes and macrophages (Yap et al 2017). In this regard, Rangasamy et al showed that the knockout of the MCP‐1 gene in diabetic mice had an inhibitory effect on modifications of the BRB (Rangasamy et al 2012).…”

Section: Therapeutic Targets and Clinical Outcomesmentioning

confidence: 99%

Monocyte chemoattractant protein-1 (MCP-1/CCL2) in diabetic retinopathy: latest evidence and clinical considerations

Taghavi

Hassanshahi

Kounis

et al. 2019

J. Cell Commun. Signal.

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Diabetic retinopathy (DR) is considered as a diabetes-related complication that can render severe visual impairments and is also a risk factor for acquired blindness in both developed as well as developing countries. Through fibrovascular epiretinal membranes (ERMs), this condition can similarly lead to tractional retinal detachment. Laboratory efforts evaluating the DR pathogenesis can be provided by ocular vitreous fluid and ERMs resulting from vitrectomy. The clinical stages of DR are significantly associated with expression levels of certain chemokines, including monocyte chemotactic protein-1 (MCP-1) in the intraocular fluid. The MCP-1 is also a known potent chemotactic factor for monocytes and macrophages that can stimulate them to produce superoxide and other mediators. Following hyperglycemia, retinal pigmented epithelial (RPE) cells, endothelial cells, and Müller's glial cells are of utmost importance for MCP-1 production, and vitreous MCP-1 levels rise in patients with DR. Increased expression of the MCP-1 in the eyes can also play a significant role in the pathogenesis of DR. In this review, current clinical and laboratory progress achieved on the MCP-1 and the DR concerning neovascularization and inflammatory responses in vitreous and/or aqueous humor of DR patients was summarized. It was suggested that further exploration of the MCP-1/CCR2 axis association between clinical stages of DR and expression levels of inflammatory and angiogenic cytokines and chemokines, principally the MCP-1 might lead to potential therapies aiming at neutralizing antibodies and viral vectors.

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“…Monocyte chemoattractant protein-1 (MCP-1) is a strong chemokine that is capable of stimulating leucocytes, particularly macrophages and monocytes. A recent study demonstrated that MCP-1 plays an important role in the inflammatory process in diabetic nephropathy (Yap 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Bee gomogenat rescues lymphoid organs from degeneration by regulating the crosstalk between apoptosis and autophagy in streptozotocin-induced diabetic mice

Badr

Sayed

Omar

et al. 2022

Environ Sci Pollut Res

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Diabetes mellitus (DM) is a metabolic disorder that causes severe complications in several tissues due to redox imbalances, which in turn cause defective angiogenesis in response to ischemia and activate a number of proinflammatory pathways. Our study aimed to investigate the effect of bee gomogenat (BG) dietary supplementation on the architecture of immune organs in a streptozotocin (STZ)-induced type 1 diabetes (T1D) mouse model. Three animal groups were used: the control non-diabetic, diabetic, and BG-treated diabetic groups. STZ-induced diabetes was associated with increased levels of blood glucose, ROS, and IL-6 and decreased levels of IL-2, IL-7, IL-4, and GSH. Moreover, diabetic mice showed alterations in the expression of autophagy markers (LC3, Beclin-1, and P62) and apoptosis markers (Bcl-2 and Bax) in the thymus, spleen, and lymph nodes. Most importantly, the phosphorylation level of AKT (a promoter of cell survival) was significantly decreased, but the expression levels of MCP-1 and HSP-70 (markers of inflammation) were significantly increased in the spleen and lymph nodes in diabetic mice compared to control animals. Interestingly, oral supplementation with BG restored the levels of blood glucose, ROS, IL-6, IL-2, IL-4, IL-7, and GSH in diabetic mice. Treatment with BG significantly abrogated apoptosis and autophagy in lymphoid organs in diabetic mice by restoring the expression levels of LC3, Beclin-1, P62, Bcl-2, and Bax; decreasing inflammatory signals by downregulating the expression of MCP-1 and HSP-70; and promoting cell survival by enhancing the phosphorylation of AKT. Our data were the first to reveal the therapeutic potential of BG on the architecture of lymphoid organs and enhancing the immune system during T1D.

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Review Article - MCP-1: A Potential Target for Diabetic Microvascular Complications?

Cited by 3 publications

References 27 publications

Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation

Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation

Monocyte chemoattractant protein-1 (MCP-1/CCL2) in diabetic retinopathy: latest evidence and clinical considerations

Bee gomogenat rescues lymphoid organs from degeneration by regulating the crosstalk between apoptosis and autophagy in streptozotocin-induced diabetic mice

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