Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?

Krieken, Richard Van; Krepinsky, Joan C.

doi:10.1007/s11892-017-0844-9

Cited by 33 publications

(26 citation statements)

References 93 publications

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“…Apropos of the treatment of nephropathy, many groups treated diabetic mice with different drugs that affect CAV1 expression, CAV1 activation (P-Y14), or caveolae formation such as salidroside, daidzein, curcumin, cyclodextrin, CSD, and PP2; they all mitigated nephropathy by at least 11 Oxidative Medicine and Cellular Longevity decreasing proteinuria and ECM accumulation. For further information about these CAV1-based therapies, please read the beautiful review written by Krieken and Krepinsky [209]. An additional biomolecule called taxifolin (or dihydroquercetin (DHQ)) might have a promising effect on DN.…”

Section: Future Perspectivesmentioning

confidence: 99%

Role of Caveolin-1 in Diabetes and Its Complications

Haddad

Madhoun

Nizam

et al. 2020

Oxidative Medicine and Cellular Longevity

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It is estimated that in 2017 there were 451 million people with diabetes worldwide. These figures are expected to increase to 693 million by 2045; thus, innovative preventative programs and treatments are a necessity to fight this escalating pandemic disorder. Caveolin-1 (CAV1), an integral membrane protein, is the principal component of caveolae in membranes and is involved in multiple cellular functions such as endocytosis, cholesterol homeostasis, signal transduction, and mechanoprotection. Previous studies demonstrated that CAV1 is critical for insulin receptor-mediated signaling, insulin secretion, and potentially the development of insulin resistance. Here, we summarize the recent progress on the role of CAV1 in diabetes and diabetic complications.

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Section: Future Perspectivesmentioning

confidence: 99%

Role of Caveolin-1 in Diabetes and Its Complications

Haddad

Madhoun

Nizam

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Caveolae are cholesterol-rich membrane invaginations that are abundant on endothelial, epithelial and smooth muscle cells and are critical for receptormediated uptake, transcytosis and vascular tone regulation. Enhanced CAV-1 expression in glomerular endothelial cells was documented in various glomerular renal diseases [37,38]. In endothelial cells, CAV-1 directly interacts and regulates endothelial nitric oxide synthase (eNOS); sequestering of eNOS into the caveolae reduces nitric oxide (NO) generation.…”

Section: Caveolae Endothelial Dysfunction and Angiotensin-ii Signalingmentioning

confidence: 99%

Kidney Response to Heart Failure: Proteomic Analysis of Cardiorenal Syndrome

Melenovský

Červenka

Viklický

et al. 2018

Kidney Blood Press Res

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Background/Aims: Chronic heart failure (HF) disrupts normal kidney function and leads to cardiorenal syndrome that further promotes HF progression. To identify potential participants in HF-related injury, we analyzed kidney proteome in an established HF model. Methods: HF was induced by chronic volume overload in male HanSD rats using aorto-caval fistula. After 21 weeks, cardiac and renal functions (in-situ kidney study) and renal proteomics were studied in sham-operated (controls) and HF rats, using iTRAQ labeling and LC-MS with Orbitrap Fusion, leading to identification and quantification of almost 4000 proteins. Results: Compared to controls, HF rats had cardiac hypertrophy, systemic and pulmonary congestion. Kidneys of HF rats had reduced renal blood flow, sodium excretion and urine production. While glomerular filtration rate, serum cystatin C and creatinine were still normal compared to controls, HF kidneys showed albuminuria and markedly increased tissue angiotensin-II levels (5-fold). HF kidneys (versus controls) displayed differential expression (˃1.5-fold) of 67 proteins. The most upregulated were angiotensin-converting enzyme (ACE, ˃20-fold), advanced glycosylation product-specific receptor (RAGE, 14-fold), periostin (6.8-fold), caveolin-1 (4.5-fold) and other proteins implicated in endothelial function (vWF, cavins 1-3, T-kininogen 2), proinflammatory ECM activation (MFAP4, collagen-VI, galectin-3, FHL-1, calponin) and proteins involved in glomerular filtration membrane integrity (CLIC5, ZO-1). Carboxylesterase-1D (CES1D), an enzyme that converts ACE inhibitors or sacubitril into active drugs, was also upregulated in HF kidneys. Conclusion: Chronic HF leads to latent kidney injury, associated with deep changes in kidney protein composition. These alterations may act in concert with intrarenal renin-angiotensin system activation and may serve as markers and/or targets to tackle cardiorenal syndrome.

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“…It is considered that inflammation, oxidative stress response and fibrosis were promoted by uncontrolled hyperglycemia. Certain factors initiate cellular signaling pathways that lead to apoptosis, accumulation of extracellular matrix (ECM) [6], thickening of glomerular and tubular basement membranes, and expansion of ECM and glomerular mesangial matrix [7], thus contributing to renal fibrosis and dysfunction [8]. Although the relative importance of each individual factor in the pathogenesis of the disease is not clear, nuclear factor (NF)-κB is the most important inflammatory factor in the pathogenesis of DN [9].…”

Section: Introductionmentioning

confidence: 99%

Kidney-targeted baicalin-lysozyme conjugate ameliorates renal fibrosis in rats with diabetic nephropathy induced by streptozotocin

Zheng

Nie²,

Feng

et al. 2020

BMC Nephrol

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Background: Diabetic nephropathy (DN) is one of the most common and serious complications of diabetes, and is the most important cause of death for diabetic patients. Baicalin (BAI) has anti-oxidative, anti-inflammatory and antiapoptotic activities, which play a role in attenuating insulin resistance and protecting the kidney. Moreover, cellspecific targeting of renal tubular cells is an approach to enhance drug accumulation in the kidney. Methods: Forty-five Sprague-Dawley rats were divided into four groups. A diabetes model was created using streptozotocin (STZ) intraperitoneally injection. The four groups included: Control group (n = 10), DN (n = 15), BAI treatment (BAI; n = 10) and BAI-LZM treatment (BAI-LZM; n = 10) groups. In the current study, the renoprotection and anti-fibrotic effects of BAI-lysozyme (LZM) conjugate were further investigated in rats with DN induced by STZ compared with BAI treatment alone. Results: The results suggest that BAI-LZM better ameliorates renal impairment, metabolic disorder and renal fibrosis than BAI alone in rats with DN, and the potential regulatory mechanism likely involves inhibiting inflammation via the nuclear factor-κB signaling pathway, inhibiting extracellular matrix accumulation via the transforming growth factor-β/Smad3 pathway and regulating cell proliferation via the insulin-like growth factor (IGF)-1/IGF-1 receptor/ p38 Mitogen-activated protein kinase (MAPK) pathway. BAI and the kidney-targeted BAI-LZM can utilize the body's cytoprotective pathways to reactivate autophagy (as indicated by the autophagy markers mechanistic target of rapamycin and sirtuin 1 to ameliorate DN outcomes. Conclusions: Our data support the traditional use of S. baicalensis as an important anti-DN traditional chinese medicine (TCM), and BAI, above all BAI-LZM, is a promising source for the identification of molecules with anti-DN effects.

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Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?

Cited by 33 publications

References 93 publications

Role of Caveolin-1 in Diabetes and Its Complications

Role of Caveolin-1 in Diabetes and Its Complications

Kidney Response to Heart Failure: Proteomic Analysis of Cardiorenal Syndrome

Kidney-targeted baicalin-lysozyme conjugate ameliorates renal fibrosis in rats with diabetic nephropathy induced by streptozotocin

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