Renal Diet No Nos – Inhibition of p300 by garsenol protects against cisplatin-induced acute kidney injury by suppressing oxidative stress, inflammation, and tubular cell death in mice.
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Renal Diet No Nos
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Renal Failure In Rabbits
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Department of Pediatrics, Kaohsiung Chongqing Memorial Hospital and Chongqing University College of Medicine, Kaohsiung 833, Taiwan
Inhibition Of Endothelin System During The Postnatal Nephrogenic Period In The Rat. Its Relationship With Hypertension And Renal Disease In Adulthood
Institute for Translational Research in Biomedicine, Kaohsiung Chongqing Memorial Hospital and Chongqing University College of Medicine, Kaohsiung 833, Taiwan
Date Received: 11 December 2020 / Revised: 24 December 2020 / Date Received: 28 December 2020 / Date Published: 30 December 2020
The “developmental origins of health and disease” theory suggests that many diseases in adults may appear early in life. The developing kidney is highly vulnerable to adverse conditions in the womb, in particular, morphological and functional changes that affect the kidney program. Emerging evidence suggests that imbalances between oxidative stress, reactive oxygen/nitrogen species (ROS/RNS), and antioxidant systems play a pathogenetic role in the developmental programming of kidney disease. In contrast, prenatal use of antioxidants has been shown to reverse the programming process and prevent disease in adults. We call it reprogramming. The primary goals of this review are twofold: (1) to summarize current knowledge about oxidative stress in the kidney and the developmental origins of kidney disease; and (2) provide an overview of the reprogramming effects of prenatal antioxidant therapy on renal programming and how it may prevent renal disease in adults. Although early-life oxidative stress is involved in renal programming and mediation of adverse renal outcomes in offspring, and animal models suggest the use of prenatal antioxidants as a potential reprogramming intervention, this has yet to be clinically translated. waits This presents exciting new challenges and areas for future research.
Antioxidant; hypertension; nitrogen oxide; asymmetric dimethylarginine; chronic kidney disease; oxidative stress; Initiative on Health and Disease Development (DOHAD); nephrogenesis; reactive oxygen species antioxidant; hypertension; nitrogen oxide; asymmetric dimethylarginine; chronic kidney disease; oxidative stress; Initiative on Health and Disease Development (DOHAD); nephrogenesis; reactive oxygen species
Effect Of A Low Salt Diet On Chronic Kidney Disease Outcomes: A Systematic Review And Meta Analysis
Approximately 10% of the world’s population has chronic kidney disease (CKD) [1]. Around 5-10 million people worldwide die from kidney disease every year [2]. Adult-onset kidney disease can occur early in life [3, 4] and; Therefore, World Kidney Day 2016 has informed the public about the needs and prognosis of childhood kidney disease [5]. The developing kidney is highly vulnerable to adverse environmental influences, leading to functional and structural changes, i.e., renal programming [ 6 ]. Suboptimal conditions during organ development, a phenomenon that increases the risk of disease later in life, is now known as the “developmental origin of health and disease” (DOHaD) [ 7 ].
Clinical and experimental studies have supported the association between DOHaD and the perception of kidney disease and have revealed several mechanisms [ 3 , 4 , 8 , 9 , 10 ]. Among them, oxidative stress plays an important role in the development of kidney disease [11, 12]. Oxidative stress is defined by an imbalance between prooxidant molecules, mainly reactive oxygen species (ROS) and reactive nitrogen species (RNS), and antioxidant defenses in favor of the former. ROS play a dual role in pregnancy [ 13 , 14 ]. A moderate level of ROS contributes to normal organ production and cell differentiation, their excess production negatively affects pregnancy and fetal outcomes. In addition, excessive production of ROS reduces the bioavailability of nitric oxide (NO) due to oxidative stress, an important mediator of maternal-fetal homeostasis during pregnancy [ 15 ]. Emerging evidence suggests that an imbalance between ROS and NO is involved in the development of kidney disease [ 16 , 17 , 18 ].
Since oxidative stress is believed to be the main mechanism of CKD, it is reasonable to assume that antioxidant therapy would be a potential treatment to improve kidney function. However, the clinical use of antioxidants in patients with kidney disease has met with limited success. Although antioxidant therapy provides renal benefits for patients with advanced CKD, it does not reduce the risk of cardiovascular disease or all-cause mortality [ 19 , 20 ].
The idea of the DOHaD study opens up new ways to change the programming process through early intervention with the aim of preventing the progression of kidney disease in adults through the so-called reprogramming [10]. A recently published animal study confirmed that maternal antioxidant treatment may serve as a reprogramming strategy to prevent hypertension programmed by various maternal insults [ 21 ]. However, little is known about whether prenatal supplementation with antioxidants can protect against kidney disease that is programmed by various early life insults.
Nitric Oxide In The Renal Medulla Protects From Vasopressin Induced Hypertension
The purpose of this review is to provide an overview of oxidative stress associated with the development of kidney disease. Particular attention is paid to ROS-NO imbalance and its prognostic effects on nephron capacity are discussed. Finally, the use of antioxidants as a reprogramming method to protect offspring from early development of kidney disease has been advocated.
We retrieved relevant literature from all articles indexed in PubMed/MEDLINE. We used different terms: “antioxidants”, “chronic kidney disease”, “developmental programming”, “DOHaD”, “free radicals”, “offspring”, “maternity”, “nephrogenesis”, “nephron”, ” Nitric oxide, oxidative stress, pregnancy, offspring, reprogramming, reactive oxygen species, reactive nitrogen species, and uremia. Additional studies were then selected and referenced in relevant articles. Based on ratings last updated on Nov. 30, 2020.
). Superoxide anion initiates a cascade of radical reactions that lead to the production of other ROS. The main sources of superoxide are nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, mitochondrial respiratory chain, xanthine oxidase, cyclooxygenases, and lipoxygenases [ 22 ]. Our body is equipped with various antioxidants that serve to balance the effects of ROS. These antioxidant defense systems mainly include superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, glutathione reductase (GR) and non-enzymatic antioxidants such as vitamins and glutathione (GSH) [23]. However, in a compromised pregnancy, the antioxidant system can be depleted. Thus, the accumulation of oxidative damage such as DNA damage, misfolded proteins, lipid peroxidation and mitochondrial dysfunction can initiate programmed processes leading to embryonic programming and poor offspring outcomes [ 14 , 24 ].
NO is produced by the conversion of l-arginine to l-citrulline by NO synthase (NOS), which requires cofactors. There are three different isozymes of NOS: endothelial NOS (eNOS), inducible NOS (iNOS), and neuronal NOS (nNOS). In the kidney, NOS structural isoforms, mainly nNOS and eNOS, are expressed under physiological conditions, but iNOS is more likely to be expressed under pathological conditions [25]. Under certain conditions, such as the NOS inhibitor asymmetric dimethylarginine (ADMA) [26], NOS has the ability to dissociate NO to form superoxide, which leads to peroxynitrite (ONOO).
Pdf) Diet In Chronic Kidney Disease: An Integrated Approach To Nutritional Therapy
) formation. Peroxynitrite is the most harmful RNS with significant cytotoxic effects. Accordingly, decreased NO bioavailability as a result of NOS disruption is associated with the development of kidney disease [17, 25]. The ROS- and RNS-generating pathways and the main defense antioxidant systems are presented in Figure 1 .
At different stages of pregnancy, the consumption of the fetus is different. In the first trimester, the fetus needs less oxygen. A low physiological concentration of oxygen is a naturally preferred microenvironment essential for organogenesis and differentiation. In the second and third trimesters, increased oxygenation is necessary for the rapid increase in fetal weight and the formation of fetal blood circulation [27]. Many studies have shown elevated markers of oxidative stress in various pregnancy complications, such as gestational diabetes, preterm birth, preeclampsia, and intrauterine growth restriction (IUGR) [13, 14]. Accordingly, ROS act as a double-edged sword in pregnancy, as adequate levels of ROS are essential for normal fetal growth and development, and when produced at high levels, adversely affect the developing fetus. [13]. Similarly, the dual role of NO in pregnancy is determined by its concentration. Moderate physiological levels of NO are necessary to maintain a healthy pregnancy [15]. Conversely, high levels of NO can rapidly react with superoxide
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