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

Diabetic Complications and Oxidative Stress: A 20-Year Voyage Back in Time and Back to the Future DOI Creative Commons
Carla Iacobini, Martina Vitale, Carlo Pesce

и другие.

Antioxidants, Год журнала: 2021, Номер 10(5), С. 727 - 727

Опубликована: Май 5, 2021

Twenty years have passed since Brownlee and colleagues proposed a single unifying mechanism for diabetic complications, introducing turning point in this field of research. For the first time, reactive oxygen species (ROS) were identified as causal link between hyperglycemia four seemingly independent pathways that are involved pathogenesis diabetes-associated vascular disease. Before after milestone diabetes research, hundreds articles describe role ROS, but failure clinical trials to demonstrate antioxidant benefits some recent experimental studies showing ROS dispensable complications call time reflect. This twenty-year journey focuses on most relevant literature regarding main sources generation their cell dysfunction complications. To identify future research directions, review discusses evidence favor against oxidative stress an initial event cellular biochemical abnormalities induced by hyperglycemia. It also explores possible alternative mechanisms, including carbonyl Warburg effect, linking glucose lipid excess, mitochondrial dysfunction, activation metabolism leading injury inflammation.

Язык: Английский

Процитировано

113
Renal metabolism and hypertension DOI Creative Commons
Zhongmin Tian, Mingyu Liang

Nature Communications, Год журнала: 2021, Номер 12(1)

Опубликована: Фев. 11, 2021

Abstract Hypertension is a leading risk factor for disease burden worldwide. The kidneys, which have high specific metabolic rate, play an essential role in the long-term regulation of arterial blood pressure. In this review, we discuss emerging renal metabolism development hypertension. Renal energy and substrate characterized by several important and, some cases, unique features. Recent advances suggest that alterations may result from genetic abnormalities or serve initially as physiological response to environmental stressors support tubular transport, ultimately affect regulatory pathways lead unfavorable cellular pathophysiological consequences contribute

Язык: Английский

Процитировано

108
Oxidative stress and the role of redox signalling in chronic kidney disease DOI
Seiji Kishi, Hajime Nagasu, Kengo Kidokoro

и другие.

Nature Reviews Nephrology, Год журнала: 2023, Номер 20(2), С. 101 - 119

Опубликована: Окт. 19, 2023

Язык: Английский

Процитировано

98
Typhaneoside-Tetrahedral Framework Nucleic Acids System: Mitochondrial Recovery and Antioxidation for Acute Kidney Injury treatment DOI
Ran Yan, Weitong Cui, Wenjuan Ma

и другие.

ACS Nano, Год журнала: 2023, Номер 17(9), С. 8767 - 8781

Опубликована: Апрель 14, 2023

Acute kidney injury (AKI) is not only a worldwide problem with cruel hospital mortality rate but also an independent risk factor for chronic disease and promoting its progression. Despite supportive therapeutic measures, there no effective treatment AKI. This study employs tetrahedral framework nucleic acid (tFNA) as vehicle combines typhaneoside (Typ) to develop the tFNA-Typ complex (TTC) treating With precise targeting ability on mitochondria renal tubule, increased antiapoptotic antioxidative effect, promoted function restoration, TTC represents promising nanomedicine AKI treatment. Overall, this has developed dual-targeted nanoparticle enhanced effects could have critical clinical applications in future.

Язык: Английский

Процитировано

83
Mitochondrial oxidative damage reprograms lipid metabolism of renal tubular epithelial cells in the diabetic kidney DOI Creative Commons
Yanjuan Hou, E.H. Tan, Honghong Shi

и другие.

Cellular and Molecular Life Sciences, Год журнала: 2024, Номер 81(1)

Опубликована: Янв. 11, 2024

Abstract The functional and structural changes in the proximal tubule play an important role occurrence development of diabetic kidney disease (DKD). Diabetes-induced metabolic changes, including lipid metabolism reprogramming, are reported to lead state tubular epithelial cells (TECs), among all disturbances metabolism, mitochondria serve as central regulators. Mitochondrial dysfunction, accompanied by increased production mitochondrial reactive oxygen species (mtROS), is considered one primary factors causing injury. Most studies have discussed how altered flux drives oxidative stress during DKD. In present study, we focused on targeting damage upstream factor abnormalities under conditions TECs. Using SS31, a tetrapeptide that protects cristae structure, demonstrated contributes TEC injury peroxidation caused accumulation. Mitochondria protected using SS31 significantly reversed decreased expression key enzymes regulators fatty acid oxidation (FAO), but had no obvious effect major glucose rate-limiting enzymes. facilitated renal Sphingosine-1-phosphate (S1P) deposition limited elevated Acer1, S1pr1 SPHK1 activity, Spns2 expression. These data suggest unbalanced droplet (LD) formulation, peroxidation, impaired FAO sphingolipid homeostasis An vitro study high drove cytosolic phospholipase A2 (cPLA2), which, turn, was responsible for LD generation S1P accumulation, HK-2 cells. A mitochondria-targeted antioxidant inhibited activation cPLA2f isoforms. Taken together, these findings identify mechanistic links between reprogrammed TECs, provide further evidence nephroprotective effects via influencing pathways.

Язык: Английский

Процитировано

35
Revitalizing Ancient Mitochondria with Nano‐Strategies: Mitochondria‐Remedying Nanodrugs Concentrate on Disease Control DOI

Xingyu Long,

Min Liu,

Yayun Nan

и другие.

Advanced Materials, Год журнала: 2024, Номер 36(18)

Опубликована: Янв. 15, 2024

Abstract Mitochondria, widely known as the energy factories of eukaryotic cells, have a myriad vital functions across diverse cellular processes. Dysfunctions within mitochondria serve catalysts for various diseases, prompting widespread demise. Mounting research on remedying damaged indicates that constitute valuable target therapeutic intervention against diseases. But less clinical practice and lower recovery rate imply limitation traditional drugs, which need further breakthrough. Nanotechnology has approached favorable regiospecific biodistribution high efficacy by capitalizing excellent nanomaterials targeting drug delivery. Mitochondria‐remedying nanodrugs achieved ideal effects. This review elucidates significance in cells organs, while also compiling mortality data related Correspondingly, nanodrug‐mediate strategies applicable mitochondria‐remedying disease are detailed, with full understanding roles dysfunction advantages nanodrugs. In addition, future challenges directions discussed. conclusion, this provides comprehensive insights into design development nanodrugs, aiming to help scientists who desire extend their fields engage interdisciplinary subject.

Язык: Английский

Процитировано

32
Gut microbial metabolites SCFAs and chronic kidney disease DOI Creative Commons
He Meng,

Wenqian Wei,

Yichen Zhang

и другие.

Journal of Translational Medicine, Год журнала: 2024, Номер 22(1)

Опубликована: Фев. 18, 2024

The global incidence of Chronic Kidney Disease (CKD) is steadily escalating, with discernible linkage to the intricate terrain intestinal microecology. microbiota orchestrates a dynamic equilibrium in organism, metabolizing dietary-derived compounds, process which profoundly impacts human health. Among these short-chain fatty acids (SCFAs), result from microbial metabolic processes, play versatile role influencing host energy homeostasis, immune function, and intermicrobial signaling, etc. SCFAs emerge as pivotal risk factors CKD's development prognosis. This paper review elucidates impact gut metabolites, specifically SCFAs, on CKD, highlighting their modulating inflammatory responses, oxidative stress, cellular autophagy, milieu, signaling cascades. An in-depth comprehension interplay between kidney disease pathogenesis may pave way for utilization biomarkers CKD progression prognosis or novel adjunctive therapeutic strategies.

Язык: Английский

Процитировано

26
VDR regulates mitochondrial function as a protective mechanism against renal tubular cell injury in diabetic rats DOI Creative Commons
Hong Chen, Hao Zhang, Aimei Li

и другие.

Redox Biology, Год журнала: 2024, Номер 70, С. 103062 - 103062

Опубликована: Янв. 26, 2024

To investigate the regulatory effect and mechanism of Vitamin D receptor (VDR) on mitochondrial function in renal tubular epithelial cell under diabetic status.

Язык: Английский

Процитировано

23
Mitochondrial dysfunction and therapeutic perspectives in osteoporosis DOI Creative Commons
Jialing Liu,

Zhonghua Gao,

Xiangjie Liu

и другие.

Frontiers in Endocrinology, Год журнала: 2024, Номер 15

Опубликована: Фев. 2, 2024

Osteoporosis (OP) is a systemic skeletal disorder characterized by reduced bone mass and structural deterioration of tissue, resulting in heightened vulnerability to fractures due increased fragility. This condition primarily arises from an imbalance between the processes resorption formation. Mitochondrial dysfunction has been reported potentially constitute one most crucial mechanisms influencing pathogenesis osteoporosis. In essence, mitochondria play role maintaining delicate equilibrium formation resorption, thereby ensuring optimal health. Nevertheless, disruption this balance can arise as consequence mitochondrial dysfunction. dysfunctional mitochondria, electron transport chain (ETC) becomes uncoupled, ATP synthesis generation reactive oxygen species (ROS). Reinforcement further exacerbated accumulation aberrant mitochondria. review, we investigated analyzed correlation dysfunction, encompassing DNA (mtDNA) alterations, oxidative phosphorylation (OXPHOS) impairment, mitophagy dysregulation, defects biogenesis dynamics, well excessive ROS accumulation, with regards OP ( Figure 1 ). Furthermore, explore prospective strategies currently available for modulating ameliorate Undoubtedly, certain therapeutic still require investigation ensure their safety efficacy clinical treatments. However, perspective, potential establishing effective safe approaches osteoporosis appears promising.

Язык: Английский

Процитировано

20
Bioorthogonal photocatalytic proximity labeling in primary living samples DOI Creative Commons
Ziqi Liu,

Fuhu Guo,

Yufan Zhu

и другие.

Nature Communications, Год журнала: 2024, Номер 15(1)

Опубликована: Март 28, 2024

Abstract In situ profiling of subcellular proteomics in primary living systems, such as native tissues or clinic samples, is crucial for understanding life processes and diseases, yet challenging due to methodological obstacles. Here we report CAT-S, a bioorthogonal photocatalytic chemistry-enabled proximity labeling method, that expands wide range samples mitochondrial proteomes. Powered by our thioQM warhead development targeted chemistry, CAT-S enables the proteins cells with high efficiency specificity. We apply diverse cell cultures, dissociated mouse well T from human blood, portraying native-state proteomic characteristics, unveiled hidden (PTPN1, SLC35A4 uORF, TRABD). Furthermore, allows quantification perturbations on dysfunctional tissues, exampled diabetic kidneys, revealing alterations lipid metabolism may drive disease progression. Given advantages non-genetic operation, generality, spatiotemporal resolution, open exciting avenues investigations are otherwise inaccessible.

Язык: Английский

Процитировано

19