Iron Deficiency in Heart Failure: Mechanisms and Pathophysiology DOI Open Access
Ridha I.S. Alnuwaysir, Martijn F. Hoes, Dirk J. van Veldhuisen

и другие.

Journal of Clinical Medicine, Год журнала: 2021, Номер 11(1), С. 125 - 125

Опубликована: Дек. 27, 2021

Iron is an essential micronutrient for a myriad of physiological processes in the body beyond erythropoiesis. deficiency (ID) common comorbidity patients with heart failure (HF), prevalence reaching up to 59% even non-anaemic patients. ID impairs exercise capacity, reduces quality life, increases hospitalisation rate and mortality risk regardless anaemia. Intravenously correcting has emerged as promising treatment HF it been shown alleviate symptoms, improve life capacity reduce hospitalisations. However, pathophysiology remains poorly characterised. Recognition triggered more research aim explain how improves status well underlying causes first place. In past few years, significant progress made understanding iron homeostasis by characterising role iron-regulating hormone hepcidin, effects on skeletal cardiac myocytes, kidneys immune system. this review, we summarise current knowledge recent advances failure, deleterious systemic cellular consequences ID.

Язык: Английский

Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications DOI Creative Commons

Qingzheng Kang,

Chunxue Yang

Redox Biology, Год журнала: 2020, Номер 37, С. 101799 - 101799

Опубликована: Окт. 1, 2020

Oxidative stress, a cytopathic outcome of excessive generation ROS and the repression antioxidant defense system for elimination, is involved in pathogenesis multiple diseases, including diabetes its complications. Retinopathy, microvascular complication diabetes, primary cause acquired blindness diabetic patients. stress has been verified as one critical contributor to retinopathy. can both contribute result from metabolic abnormalities induced by hyperglycemia, mainly increased flux polyol pathway hexosamine pathway, hyper-activation protein kinase C (PKC) isoforms, accumulation advanced glycation end products (AGEs). Moreover, hyperglycemia-mediated epigenetic modification also leads imbalance between scavenging production ROS. Excessive induces mitochondrial damage, cellular apoptosis, inflammation, lipid peroxidation, structural functional alterations retina. Therefore, it important understand elucidate oxidative stress-related mechanisms underlying progress In addition, correlated with provide potential therapeutic targets develop safe effective treatments Here, we summarized main strategies control this disease.

Язык: Английский

Процитировано

731

Mitochondrial quality control in kidney injury and repair DOI
Chengyuan Tang, Juan Cai,

Xiao-Ming Yin

и другие.

Nature Reviews Nephrology, Год журнала: 2020, Номер 17(5), С. 299 - 318

Опубликована: Ноя. 24, 2020

Язык: Английский

Процитировано

338

Crosstalk between mitochondrial dysfunction, oxidative stress, and age related neurodegenerative disease: Etiologies and therapeutic strategies DOI
Hasnaa A. Elfawy, Biswadeep Das

Life Sciences, Год журнала: 2018, Номер 218, С. 165 - 184

Опубликована: Дек. 20, 2018

Язык: Английский

Процитировано

292

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities DOI Open Access
Lucas Opazo-Ríos, Sebastián Mas,

Gema Marín‐Royo

и другие.

International Journal of Molecular Sciences, Год журнала: 2020, Номер 21(7), С. 2632 - 2632

Опубликована: Апрель 10, 2020

Lipotoxicity is characterized by the ectopic accumulation of lipids in organs different from adipose tissue. mainly associated with dysfunctional signaling and insulin resistance response non-adipose tissue such as myocardium, pancreas, skeletal muscle, liver, kidney. Serum lipid abnormalities renal have been development kidney diseases, particular diabetic nephropathy. Chronic hyperinsulinemia, often seen type 2 diabetes, plays a crucial role blood liver metabolism abnormalities, thus resulting increased non-esterified fatty acids (NEFA). Excessive alters cellular homeostasis activates lipogenic glycogenic cell-signaling pathways. Recent evidences indicate that both quantity quality are involved damage to lipotoxicity activating inflammation, oxidative stress, mitochondrial dysfunction, cell-death. The pathological effects observed cells, promoting podocyte injury, tubular damage, mesangial proliferation, endothelial activation, formation macrophage-derived foam cells. Therefore, this review examines recent preclinical clinical research about potentially harmful kidney, metabolic markers these mechanisms, major pathways affected, causes excessive accumulation, types involved, well offers comprehensive update therapeutic strategies targeting lipotoxicity.

Язык: Английский

Процитировано

254

Systemic immune-inflammation index is associated with diabetic kidney disease in Type 2 diabetes mellitus patients: Evidence from NHANES 2011-2018 DOI Creative Commons
Wencong Guo, Yancheng Song, Yan Sun

и другие.

Frontiers in Endocrinology, Год журнала: 2022, Номер 13

Опубликована: Дек. 6, 2022

Objective Diabetic kidney disease (DKD) is the most common chronic (CKD) and has highest prevalence of end-stage (ESKD) globally, owing mostly to rise in Type 2 diabetes mellitus (T2DM) correlated with obesity. Current research suggested that immune response inflammation may play a role pathophysiology T2DM. The systemic immune-inflammation index (SII) novel integrated inflammatory biomarker not yet been linked DKD. We aimed identify potential relationship between SII Methods In National Health Nutrition Examination Survey (NHANES) 2011 2018, current cross-sectional study was conducted among adults calculated as platelet count × neutrophil count/lymphocyte count. DKD diagnosed impaired glomerular filtration rate (< 60 mL/min/1.73 m assessed by using Chronic Kidney Disease Epidemiology Collaboration algorithm), albuminuria (urine albumin creatinine ratio ≥ 30 mg/g), or both T2DM patients. To investigate independent association DKD, weighted univariate multivariable logistic regression analyses subgroup were performed. Results involved 3937 patients total, whom 1510 (38.4%) had for diagnosis. After adjustment covariates, revealed high level associated increased likelihood (OR = 1.42, 95% CI: 1.10-1.83, P 0.01). Subgroup interaction tests age, gender, estimated (eGFR), urine albumin-to-creatinine (ACR), body mass (BMI), hypertension, hyperlipidemia, anti-inflammation therapy (yes no), metformin use insulin no) no significant dependence on this positive (all p >0.05). Conclusions Our results indicate higher could be cost-effective straightforward approach detecting This needs verified further prospective investigations.

Язык: Английский

Процитировано

209

Chronic Inflammation in Chronic Kidney Disease Progression: Role of Nrf2 DOI
Peter Stenvinkel, Glenn M. Chertow, Prasad Devarajan

и другие.

Kidney International Reports, Год журнала: 2021, Номер 6(7), С. 1775 - 1787

Опубликована: Май 4, 2021

Язык: Английский

Процитировано

184

Mitochondrial dysfunction in diabetic kidney disease DOI

Pascal Zhongping Wei,

Cheuk‐Chun Szeto

Clinica Chimica Acta, Год журнала: 2019, Номер 496, С. 108 - 116

Опубликована: Июль 2, 2019

Язык: Английский

Процитировано

180

AMPK agonist alleviate renal tubulointerstitial fibrosis via activating mitophagy in high fat and streptozotocin induced diabetic mice DOI Creative Commons
Yachun Han, Shiqi Tang, Yuting Liu

и другие.

Cell Death and Disease, Год журнала: 2021, Номер 12(10)

Опубликована: Окт. 9, 2021

Abstract Renal tubulointerstitial fibrosis was a crucial pathological feature of diabetic nephropathy (DN), and renal tubular injury might associate with abnormal mitophagy. In this study, we investigated the effects molecular mechanisms AMPK agonist metformin on mitophagy cellular in cell under condition. The high fat diet (HFD) streptozotocin (STZ)-induced type 2 mice model HK-2 cells were used study. Metformin administered drinking water (200 mg/kg/d) for 24 weeks. lesions, oxidative stress some indicators (e.g., LC3II, Pink1, Parkin) examined both tissue cells. Additionally, compound C (an inhibitor) Pink1 siRNA applied to explore regulation mechanism We found that expression p-AMPK, Parkin, Atg5 decreased obviously. reduced levels serum creatinine, urine protein, attenuated HFD/STZ induced mice. addition, reversed dysfunction over-expression NLRP3. vitro pretreatment inhibitor or negated beneficial metformin. Furthermore, noted activated p-AMPK promoted translocation from cytoplasm mitochondria, then occurrence HG/HFA ambience. Our results suggested first time ameliorated HFD/STZ-induced via activating through p-AMPK-Pink1-Parkin pathway.

Язык: Английский

Процитировано

149

Kidney lipid dysmetabolism and lipid droplet accumulation in chronic kidney disease DOI
Alla Mitrofanova, Sandra Merscher, Alessia Fornoni

и другие.

Nature Reviews Nephrology, Год журнала: 2023, Номер 19(10), С. 629 - 645

Опубликована: Июль 27, 2023

Язык: Английский

Процитировано

126

Challenges of fluoride pollution in environment: Mechanisms and pathological significance of toxicity – A review DOI
Shouyan Wu, Yajing Wang, Mujahid Iqbal

и другие.

Environmental Pollution, Год журнала: 2022, Номер 304, С. 119241 - 119241

Опубликована: Апрель 1, 2022

Язык: Английский

Процитировано

125