Mitochondrial DNA: A New Predictor of Diabetic Kidney Disease

Huang, Yajing; Chi, Jen-Tsan; Wei, Fanxiang; Zhou, Yue; Cao, Yihai; Wang, Yangang

doi:10.1155/2020/3650937

Cited by 15 publications

(6 citation statements)

References 65 publications

(93 reference statements)

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“…The pathological phenomenon of the MPT pore opening is characterized by a sudden loss of permeability of the inner mitochondrial membrane, which can lead to the collapse of the membrane potential, release of proapoptotic proteins from mitochondria, and ultimately cell death [ 133 ]. Finally, excessive ROS production can induce oxidative damage to mtDNA followed by deficiencies of the respiratory chain complexes and total mitochondrial dysfunction [ 134 ].…”

Section: Mechanisms Of the Diabetes-induced Mitochondrial Dysfunctmentioning

confidence: 99%

Diabetes Mellitus, Mitochondrial Dysfunction and Ca2+-Dependent Permeability Transition Pore

Belosludtsev

Belosludtseva

Dubinin

2020

IJMS

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Diabetes mellitus is one of the most common metabolic diseases in the developed world, and is associated either with the impaired secretion of insulin or with the resistance of cells to the actions of this hormone (type I and type II diabetes, respectively). In both cases, a common pathological change is an increase in blood glucose—hyperglycemia, which eventually can lead to serious damage to the organs and tissues of the organism. Mitochondria are one of the main targets of diabetes at the intracellular level. This review is dedicated to the analysis of recent data regarding the role of mitochondrial dysfunction in the development of diabetes mellitus. Specific areas of focus include the involvement of mitochondrial calcium transport systems and a pathophysiological phenomenon called the permeability transition pore in the pathogenesis of diabetes mellitus. The important contribution of these systems and their potential relevance as therapeutic targets in the pathology are discussed.

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Section: Mechanisms Of the Diabetes-induced Mitochondrial Dysfunctmentioning

confidence: 99%

Diabetes Mellitus, Mitochondrial Dysfunction and Ca2+-Dependent Permeability Transition Pore

Belosludtsev

Belosludtseva

Dubinin

2020

IJMS

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“…These show that Forsythiaside has anti-oxidation (Huang et al, 2015), anti-inflammation , and immunoregulatory (Cheng et al, 2014) properties. Studies have shown that one of the core mechanisms of DKD development is the accumulation of ROS, inflammatory factors, and immune complexes in the kidney, which further activate cytotoxic signaling in the kidney, leading to renal dysfunction (Huang et al, 2020). Forsythiaside may protect against DKD by intervening these mechanisms.…”

Section: Forsythiaside Suppressed the Expression Of Prkca And Rhoa In...mentioning

confidence: 99%

Cellular mechanism of action of forsythiaside for the treatment of diabetic kidney disease

Miao

Chen

et al. 2023

Front. Pharmacol.

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Background: Diabetic kidney disease (DKD) becomes the leading cause of death for end-stage renal disease, whereas the potential mechanism is unclear and effective therapy is still rare. Our study was designed to investigate the cellular mechanism of Forsythiaside against DKD.Materials and Methods: The targets of Forsythiaside and the DKD-related targets were obtained from databases. The overlapping targets in these two sets were regarded as potential targets for alleviation of DKD by Forsythiaside. The targets of diabetic podocytopathy and tubulopathy were also detected to clarify the mechanism of Forsythiaside ameliorating DKD from the cellular level.Results: Our results explored that PRKCA and RHOA were regarded as key therapeutic targets of Forsythiaside with excellent binding affinity for treating DKD podocytopathy. Enrichment analysis suggested the underlying mechanism was mainly focused on the oxidative stress and mTOR signaling pathway. The alleviated effects of Forsythiaside on the reactive oxidative species accumulation and PRKCA and RHOA proteins upregulation in podocytes were also confirmed.Conclusion: The present study elucidates that Forsythiaside exerts potential treatment against DKD which may act directly RHOA and PRKCA target by suppressing the oxidative stress pathway in podocytes. And Forsythiaside could be regarded as one of the candidate drugs dealing with DKD in future experimental or clinical researches.

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“…Their group found out that mtDNA was lower in diabetic patients with macroalbuminuria than in patients with microalbuminuria or normalbuminuria. Therefore, altered mtDNA content can predict the occurrence of DKD and the oxidative stress environment [ 84 ]. Interestingly, release of mtDNA under cellular stress has been previously considered as a damage-associated molecular pattern (DAMP) [ 85 ].…”

Section: Oxidative Stress In Diabetic Kidney Disease: Contribution Of Sodium Glucose Co-transporter Type 2 (Sglt2)mentioning

confidence: 99%

Antioxidant Roles of SGLT2 Inhibitors in the Kidney

et al. 2022

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The reduction-oxidation (redox) system consists of the coupling and coordination of various electron gradients that are generated thanks to serial reduction-oxidation enzymatic reactions. These reactions happen in every cell and produce radical oxidants that can be mainly classified into reactive oxygen species (ROS) and reactive nitrogen species (RNS). ROS and RNS modulate cell-signaling pathways and cellular processes fundamental to normal cell function. However, overproduction of oxidative species can lead to oxidative stress (OS) that is pathological. Oxidative stress is a main contributor to diabetic kidney disease (DKD) onset. In the kidney, the proximal tubular cells require a high energy supply to reabsorb proteins, metabolites, ions, and water. In a diabetic milieu, glucose-induced toxicity promotes oxidative stress and mitochondrial dysfunction, impairing tubular function. Increased glucose level in urine and ROS enhance the activity of sodium/glucose co-transporter type 2 (SGLT2), which in turn exacerbates OS. SGLT2 inhibitors have demonstrated clear cardiovascular benefits in DKD which may be in part ascribed to the generation of a beneficial equilibrium between oxidant and antioxidant mechanisms.

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Mitochondrial DNA: A New Predictor of Diabetic Kidney Disease

Cited by 15 publications

References 65 publications

Diabetes Mellitus, Mitochondrial Dysfunction and Ca2+-Dependent Permeability Transition Pore

Diabetes Mellitus, Mitochondrial Dysfunction and Ca2+-Dependent Permeability Transition Pore

Cellular mechanism of action of forsythiaside for the treatment of diabetic kidney disease

Antioxidant Roles of SGLT2 Inhibitors in the Kidney

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