Renoprotective effect of myricetin restrains dyslipidemia and renal mesangial cell proliferation by the suppression of sterol regulatory element binding proteins in an experimental model of diabetic nephropathy

“…Saroglitazar, a potent PPAR-a/g agonist, did not induce weight gain, peripheral edema, or other adverse events after 1 year (52) and improved markers of NAFLD in patients with diabetes (53), whereas aleglitazar slowed estimated glomerular filtration rate (eGFR) decline in diabetic nephropathy (54) ( Among various lipotoxic species accumulating in NAFLD and CKD, free cholesterol is believed to play a key pathogenic role in liver and renal injury (13,55). Ectopic cholesterol accumulation is driven by an inappropriate upregulation of transcription factor SREBP-2, with consequently increased cholesterol synthesis, influx, and retention and reduced cholesterol excretion by liver and renal cells (13,55) (Fig. 1).…”

Section: Potential Pathogenic Mechanisms Contributing To Nafld To Ckdmentioning

confidence: 99%

Fatty Liver and Chronic Kidney Disease: Novel Mechanistic Insights and Therapeutic Opportunities

et al. 2016

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Chronic kidney disease (CKD) is a risk factor for end-stage renal disease (ESRD) and cardiovascular disease (CVD). ESRD or CVD develop in a substantial proportion of patients with CKD receiving standard-of-care therapy, and mortality in CKD remains unchanged. These data suggest that key pathogenetic mechanisms underlying CKD progression go unaffected by current treatments. Growing evidence suggests that nonalcoholic fatty liver disease (NAFLD) and CKD share common pathogenetic mechanisms and potential therapeutic targets. Common nutritional conditions predisposing to both NAFLD and CKD include excessive fructose intake and vitamin D deficiency. Modulation of nuclear transcription factors regulating key pathways of lipid metabolism, inflammation, and fibrosis, including peroxisome proliferatoractivated receptors and farnesoid X receptor, is advancing to stage III clinical development. The relevance of epigenetic regulation in the pathogenesis of NAFLD and CKD is also emerging, and modulation of microRNA21 is a promising therapeutic target. Although single antioxidant supplementation has yielded variable results, modulation of key effectors of redox regulation and molecular sensors of intracellular energy, nutrient, or oxygen status show promising preclinical results. Other emerging therapeutic approaches target key mediators of inflammation, such as chemokines; fibrogenesis, such as galectin-3; or gut dysfunction through gut microbiota manipulation and incretin-based therapies. Furthermore, NAFLD per se affects CKD through lipoprotein metabolism and hepatokine secretion, and conversely, targeting the renal tubule by sodium-glucose cotransporter 2 inhibitors can improve both CKD and NAFLD. Implications for the treatment of NAFLD and CKD are discussed in light of this new therapeutic armamentarium. EPIDEMIOLOGICAL EVIDENCE LINKING NAFLD AND CKDChronic kidney disease (CKD) affects up to 8% of the world's adult population, with its prevalence increasing in an aging population beset by lifestyle-associated diseases such as obesity, the metabolic syndrome, diabetes, hypertension, and smoking (1). CKD may progress to end-stage renal disease (ESRD) and is an important cardiovascular disease (CVD) risk factor. Importantly, most patients with CKD die as a result of CVD before renal replacement therapy is initiated (1).There is potential for improving recognition and treatment of CKD. In the Third National Health and Nutrition Survey, awareness among patients with stage 3 CKD was ,8% (1). Furthermore, ESRD or CVD develop in a substantial proportion of patients with CKD receiving standard-of-care therapy, and all-cause mortality remains unchanged in the CKD population (2). These data suggest that key pathogenetic mechanisms underlying

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“…Cornus officinalis [47], curcumin [108], Fragaria × ananassa [89], myricetin [157] Transforming/tumor growth factor β (TGF-β) (-)-Epicatechin 3-O-gallate and (-)-epigallocatechin 3-O-gallate [81], Abelmoschus manihot [104], Abelmoschus manihot [156], berberine [121], berberine [85], berberine [117], berberine [118], breviscapine [51], breviscapine [52], cocoa enriched with polyphenols [110], Cordyceps militaris [114], Coreopsis tinctoria [72], curcumin [108], curcumin [79], curcumin analogue (B06) [66], Dioscorea bulbifera [96] (human), ellagic acid [37], Hypericum perforatum [31], isorhamnetin [87], moringa isothiocyanate [42], myricetin [157], Paeonia lactiflora [120], Paeonia suffruticosa [109], Panax quinquefolium [82], Prunella vulgaris [84], Psoralea corylifolia [115], Zea mays anthocyanins [70], Qidan Dihuang [119], rhein [113], Shen-Yan-Fang-Shuai Formula [80], Tangke decoction [116] p38-mitogen-activated protein kinase (p38MAPK) (-)-Epigallocatechin-3-gallate [155], Abelmoschus manihot [156], Danhong [154], emodin [ Berberine [158], berberine …”

Section: Journal Of Diabetes Researchmentioning

confidence: 99%

“…Abelmoschus manihot [104], berberine [121], berberine [85], berberine [117], cocoa enriched with polyphenols [110], Cordyceps militaris [114], Coreopsis tinctoria [72], dihydroquercetin [48], Hydrangea paniculata [59], Hypericum perforatum [31], myricetin [157], Paeonia lactiflora [120], Panax quinquefolium [82], Prunella vulgaris [84], Psoralea corylifolia [115], Zea mays anthocyanins [70], Shen-Yan-Fang-Shuai Formula [80], triptolide [133], astragaloside IV [131] Fibronectin (-)-Epicatechin 3-O-gallate and (-)-epigallocatechin 3-O-gallate [81], (+)-catechin [46], berberine [85], berberine [117], Coccinia indica [111], cocoa enriched with polyphenols [110], Coreopsis tinctoria [72], dihydroquercetin [48], ellagic acid [37], emodin [153], Hydrangea paniculata [59], Hypericum perforatum [31], myricetin [157], Paeonia suffruticosa [109], Panax quinquefolium [82], Psoralea corylifolia [115], rhein [113], Shen-Yan-Fang-Shuai Formula [80], triptolide [133] Crocin [73] Podocyte slit diaphragm proteins (nephrin, podocin, and synaptopodin) Puerarin [60] Podocin Crocin…”

Section: Hif-1α/pi3k/aktmentioning

confidence: 99%

“…Purple corn (Zea mays) anthocyanins hindered the interaction between NF-κB and canonical TGF-β1 (i.e., Smad) pathways. Consequently, it thwarted ECM expansion by both promoting ECM degradation and reducing new ECM formation as a result of TGF-β1 signaling inhibition blocking the induction of ICAM-1 and MCP-1 (responsible for connective tissue growth factor expression) and the Moringa isothiocyanate [42] 5′ adenosine monophosphate-activated protein kinase (AMPK) Cocoa enriched with polyphenols [110], Coreopsis tinctoria [72] Sirtuin 1 (SIRT1) Puerarin [76] Peroxisome proliferator-activated receptor-α (PPAR-α) Abelmoschus manihot [104], myricetin [157] Peroxisome proliferator-activated receptor-γ (PPAR-γ)…”

Section: In Vitro Studies-potentially Nephroprotectivementioning

confidence: 99%

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Mechanisms of Herbal Nephroprotection in diabetes mellitus

Dragoș

Manea

Timofte

et al. 2020

Journal of Diabetes Research

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Diabetic nephropathy (DN) is a leading cause of kidney morbidity. Despite the multilayered complexity of the mechanisms involved in the pathogenesis of DN, the conventional treatment is limited to just a few drug classes fraught with the risk of adverse events, including the progression of renal dysfunction. Phytoceuticals offer a promising alternative as they act on the many-sidedness of DN pathophysiology, multitargeting its intricacies. This paper offers a review of the mechanisms underlying the protective action of these phytoagents, including boosting the antioxidant capabilities, suppression of inflammation, averting the proliferative and sclerosing/fibrosing events. The pathogenesis of DN is viewed as a continuum going from the original offense, high glucose, through the noxious products it generates (advanced glycation end-products, products of oxidative and nitrosative stress) and the signaling chains consequently brought into action, to the harmful mediators of inflammation, sclerosis, and proliferation that eventually lead to DN, despite the countervailing attempts of the protective mechanisms. Special attention was given to the various pathways involved, pointing out the ability of the phytoagents to hinder the deleterious ones (especially those leading to, driven by, or associated with TGF-β activation, SREBP, Smad, MAPK, PKC, NF-κB, NLRP3 inflammasome, and caspase), to promote the protective ones (PPAR-α, PPAR-γ, EP4/Gs/AC/cAMP, Nrf2, AMPK, and SIRT1), and to favorably modulate those with potentially dual effect (PI3K/Akt). Many phytomedicines have emerged as potentially useful out of in vitro and in vivo studies, but the scarcity of human trials seriously undermines their usage in the current clinical practice—an issue that stringently needs to be addressed.

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Renoprotective effect of myricetin restrains dyslipidemia and renal mesangial cell proliferation by the suppression of sterol regulatory element binding proteins in an experimental model of diabetic nephropathy

Cited by 25 publications

References 50 publications

Investigation of antidiabetic action ofAntidesma buniusextract in type 1 diabetes

Investigation of antidiabetic action ofAntidesma buniusextract in type 1 diabetes

Fatty Liver and Chronic Kidney Disease: Novel Mechanistic Insights and Therapeutic Opportunities

Mechanisms of Herbal Nephroprotection in diabetes mellitus

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