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https://www.readbyqxmd.com/read/28205545/octreotide-attenuates-acute-kidney-injury-after-hepatic-ischemia-and-reperfusion-by-enhancing-autophagy
#1
Huiping Sun, Shuangfa Zou, Keith A Candiotti, Yanhua Peng, Qinya Zhang, Weiqiang Xiao, Yiyun Wen, Jiao Wu, Jinfeng Yang
Octreotide exerts a protective effect in hepatic ischemia-reperfusion (HIR) injury. However, whether octreotide preconditioning could also reduce acute kidney injury (AKI) after HIR is unknown. This study was designed to investigate the role of octreotide in AKI after HIR. Male Sprague-Dawley rats were pretreated with octreotide or octreotide combined with 3-methyladenine (autophagy inhibitor, 3MA). Plasma creatinine, inflammation markers (e.g., TNF-α and IL-6 etc.), apoptosis, autophagy and phosphorylation of protein kinase B/mammalian target of rapamycin/p70 ribosomal S6 kinase (Akt/mTOR/p70S6K) in the kidney were measured after 60 minutes of liver ischemia and 24 hours of reperfusion for each rat...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28139396/heme-oxygenase-1-as-a-therapeutic-target-in-acute-kidney-injury
#2
Subhashini Bolisetty, Abolfazl Zarjou, Anupam Agarwal
A common clinical condition, acute kidney injury (AKI) significantly influences morbidity and mortality, particularly in critically ill patients. The pathophysiology of AKI is complex and involves multiple pathways, including inflammation, autophagy, cell-cycle progression, and oxidative stress. Recent evidence suggests that a single insult to the kidney significantly enhances the propensity to develop chronic kidney disease. Therefore, the generation of effective therapies against AKI is timely. In this context, the cytoprotective effects of heme oxygenase 1 (HO-1) in animal models of AKI are well documented...
January 27, 2017: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
https://www.readbyqxmd.com/read/28003091/recycling-to-discover-something-new-the-role-of-autophagy-in-kidney%C3%A2-disease
#3
Jeremy S Leventhal, Christina M Wyatt, Michael J Ross
This year, the Nobel Prize in Physiology or Medicine was awarded to Yoshinori Ohsumi for his groundbreaking work in dissecting the mechanisms of autophagy, a cellular process resulting in the organized degradation of cytoplasmic components. Ohsumi's work paved the way for subsequent studies that demonstrated critical roles for autophagy in modulating both acute and chronic kidney injury. This work may lead to future therapeutic approaches that target the autophagy system to prevent or treat kidney diseases...
January 2017: Kidney International
https://www.readbyqxmd.com/read/27715411/the-impact-of-autophagy-on-the-development-of-senescence-in-primary-tubular-epithelial-cells
#4
Arpita Baisantry, Sagar Bhayana, Christoph Wrede, Jan Hegermann, Hermann Haller, Anette Melk, Roland Schmitt
Autophagy and senescence are 2 distinct pathways that are importantly involved in acute kidney injury and renal repair. Recent data indicate that the 2 processes might be interrelated. To investigate the potential link between autophagy and senescence in the kidney we isolated primary tubular epithelial cells (PTEC) from wild-type mice and monitored the occurrence of cellular senescence during autophagy activation and inhibition. We found that the process of cell isolation and transfer into culture was associated with a strong basal autophagic activation in PTEC...
November 2016: Cell Cycle
https://www.readbyqxmd.com/read/27498898/acute-renal-failure-a-serious-complication-in-patients-after-kidney-transplantation
#5
REVIEW
G Basta-Jovanovic, Lj Bogdanovic, M Radunovic, M Prostran, R Naumovic, S Simic-Ogrizovic, S Radojevic-Skodric
Free radical-mediated injury releases proinflammatory cytokines and activates innate immunity. It has been suggested that the early innate response and the ischemic tissue damage play roles in the development of adaptive responses, which may lead to acute kidney rejection. Various durations of hypothermic kidney storage before transplantation add to ischemic tissue damage. The final stage of ischemic injury occurs during reperfusion that develops hours or days after the initial insult. Repair and regeneration processes occur together with cellular apoptosis, autophagy and necrosis and a favorable outcome is expected if regeneration prevails...
2016: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/27380103/neutrophil-gelatinase-associated-lipocalin-worsens-ischemia-reperfusion-damage-of-kidney-cells-by-autophagy
#6
Wenjing Zhang, Shuo Yang, Liyan Cui, Jie Zhang
This study aimed to explore the influence of neutrophil gelatinase-associated lipocalin on autophagy and its role in ischemia/reperfusion injury in human kidney-2 (HK-2) cells during acute kidney injury (AKI). HK-2 cells were given hypoxia/reoxygenation treatment for different times to simulate ischemia/reperfusion injury. Autophagy was evaluated by western blot and immunofluorescence of GFP-LC3. Cell viability was tested to reflect the degree of cell damage. The autophagy inhibitor 3-MA was used to inhibit autophagy and determine the role of autophagy in ischemia/reperfusion injury...
August 2016: Renal Failure
https://www.readbyqxmd.com/read/27376761/telomerase-autophagy-and-acute-kidney-injury
#7
Raymond C Harris, Huifang Cheng
In humans, aging is associated with telomere shortening and increased susceptibility to acute kidney injury. Telomerase is essential to maintain telomere length. The fourth generation mice with telomerase deletion have progressive shortening of telomeres. Those mice delayed recovery from ischemia-reperfusion injury, due to an increase in tubule cell senescence and impairment of autophagy, the latter of which may be mediated in part by increased mTOR signaling. © 2016 S. Karger AG, Basel.
2016: Nephron
https://www.readbyqxmd.com/read/27339388/the-role-of-bcl-2-family-members-in-acute-kidney-injury
#8
REVIEW
Steven C Borkan
B-cell lymphoma 2 (BCL-2) family proteins gather at the biologic cross-roads of renal cell survival: the outer mitochondrial membrane. Despite shared sequence and structural features, members of this conserved protein family constantly antagonize each other in a life-and-death battle. BCL-2 members innocently reside within renal cells until activated or de-activated by physiologic stresses caused by common nephrotoxins, transient ischemia, or acute glomerulonephritis. Recent experimental data not only illuminate the intricate mechanisms of apoptosis, the most familiar form of BCL-2-mediated cell death, but emphasizes their newfound roles in necrosis, necroptosis, membrane pore transition regulated necrosis, and other forms of acute cell demise...
May 2016: Seminars in Nephrology
https://www.readbyqxmd.com/read/27166518/mitochondria-as-therapeutic-targets-in-acute-kidney-injury
#9
Andrew M Hall, Claus D Schuh
PURPOSE OF REVIEW: Mitochondria are complex intracellular organelles with a variety of important functions. The kidney tubule is densely packed with mitochondria, and mitochondrial dysfunction is thought to be central to the pathogenesis of acute kidney injury (AKI). Mitochondria therefore represent potential targets for novel therapeutic interventions in AKI. RECENT FINDINGS: Several mitochondrial targeted approaches have shown promise in recent preclinical studies of AKI, including measures to: reduce oxidative stress within mitochondria; prevent mitochondrial fission and activation of cell death pathways; enhance recycling of damaged mitochondria via autophagy and mitophagy; and accelerate mitochondrial biogenesis postinsult...
July 2016: Current Opinion in Nephrology and Hypertension
https://www.readbyqxmd.com/read/27153058/autophagy-innate-immunity-and-tissue-repair-in-acute-kidney-injury
#10
REVIEW
Pu Duann, Elias A Lianos, Jianjie Ma, Pei-Hui Lin
Kidney is a vital organ with high energy demands to actively maintain plasma hemodynamics, electrolytes and water homeostasis. Among the nephron segments, the renal tubular epithelium is endowed with high mitochondria density for their function in active transport. Acute kidney injury (AKI) is an important clinical syndrome and a global public health issue with high mortality rate and socioeconomic burden due to lack of effective therapy. AKI results in acute cell death and necrosis of renal tubule epithelial cells accompanied with leakage of tubular fluid and inflammation...
May 3, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27140855/long-noncoding-rnas-in-kidney-and-cardiovascular-diseases
#11
REVIEW
Johan M Lorenzen, Thomas Thum
Transcription of a large part of the human genome results in RNA transcripts that have limited or no protein-coding potential. These include long noncoding RNAs (lncRNAs), which are defined as being ≥200 nucleotides long. Unlike microRNAs, which have been extensively studied, little is known about the functional role of lncRNAs. However, studies over the past 5 years have shown that lncRNAs interfere with tissue homeostasis and have a role in pathological processes, including in the kidney and heart. The developmental expression of the microRNA sponge H19, for example, is altered in the kidneys of embryos carried by hyperglycaemic mothers, and the lncRNA Malat1 regulates hyperglycaemia-induced inflammation in endothelial cells...
June 2016: Nature Reviews. Nephrology
https://www.readbyqxmd.com/read/27108948/renoprotective-approaches-and-strategies-in-acute-kidney-injury
#12
REVIEW
Yuan Yang, Meifang Song, Yu Liu, Hong Liu, Lin Sun, Youming Peng, Fuyou Liu, Manjeri A Venkatachalam, Zheng Dong
Acute kidney injury (AKI) is a major renal disease associated with high mortality rate and increasing prevalence. Decades of research have suggested numerous chemical and biological agents with beneficial effects in AKI. In addition, cell therapy and molecular targeting have been explored for reducing kidney tissue damage and promoting kidney repair or recovery from AKI. Mechanistically, these approaches may mitigate oxidative stress, inflammation, cell death, and mitochondrial and other organellar damage, or activate cytoprotective mechanisms such as autophagy and pro-survival factors...
July 2016: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/27052588/metformin-protects-against-cisplatin-induced-tubular-cell-apoptosis-and-acute-kidney-injury-via-ampk%C3%AE-regulated-autophagy-induction
#13
Jianzhong Li, Yuan Gui, Jiafa Ren, Xin Liu, Ye Feng, Zhifeng Zeng, Weichun He, Junwei Yang, Chunsun Dai
Metformin, one of the most common prescriptions for patients with type 2 diabetes, is reported to protect the kidney from gentamicin-induced nephrotoxicity. However, the role and mechanisms for metformin in preventing cisplatin-induced nephrotoxicity remains largely unknown. In this study, a single intraperitoneal injection of cisplatin was employed to induce acute kidney injury (AKI) in CD1 mice. The mice exhibited severe kidney dysfunction and histological damage at day 2 after cisplatin injection. Pretreatment of metformin could markedly attenuate cisplatin-induced acute kidney injury, tubular cell apoptosis and inflammatory cell accumulation in the kidneys...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27048819/regulation-of-necrotic-cell-death-p53-parp1-and-cyclophilin-d-overlapping-pathways-of-regulated-necrosis
#14
REVIEW
Yuan Ying, Babu J Padanilam
In contrast to apoptosis and autophagy, necrotic cell death was considered to be a random, passive cell death without definable mediators. However, this dogma has been challenged by recent developments suggesting that necrotic cell death can also be a regulated process. Regulated necrosis includes multiple cell death modalities such as necroptosis, parthanatos, ferroptosis, pyroptosis, and mitochondrial permeability transition pore (MPTP)-mediated necrosis. Several distinctive executive molecules, particularly residing on the mitochondrial inner and outer membrane, amalgamating to form the MPTP have been defined...
2016: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/26990086/autophagy-limits-endotoxemic-acute-kidney-injury-and-alters-renal-tubular-epithelial-cell-cytokine-expression
#15
Jeremy S Leventhal, Jie Ni, Morgan Osmond, Kyung Lee, G Luca Gusella, Fadi Salem, Michael J Ross
Sepsis related acute kidney injury (AKI) is a common in-hospital complication with a dismal prognosis. Our incomplete understanding of disease pathogenesis has prevented the identification of hypothesis-driven preventive or therapeutic interventions. Increasing evidence in ischemia-reperfusion and nephrotoxic mouse models of AKI support the theory that autophagy protects renal tubular epithelial cells (RTEC) from injury. However, the role of RTEC autophagy in septic AKI remains unclear. We observed that lipopolysaccharide (LPS), a mediator of gram-negative bacterial sepsis, induces RTEC autophagy in vivo and in vitro through TLR4-initiated signaling...
2016: PloS One
https://www.readbyqxmd.com/read/26935540/nqo1-deficiency-leads-enhanced-autophagy-in-cisplatin-induced-acute-kidney-injury-through-the-ampk-tsc2-mtor-signaling-pathway
#16
Tae-Won Kim, Young-Jung Kim, Hyun-Tae Kim, Se-Ra Park, Mee-Young Lee, Yong-Deok Park, Chul-Ho Lee, Ju-Young Jung
AIMS: Recent studies have revealed that autophagy is induced under various disease conditions; however, the role of autophagy in pathological states is controversial. NAD(P)H: quinone oxidoreductase 1 (NQO1) is a highly inducible cytoprotective gene that regulates reactive oxygen species (ROS) generation. In this study, we examined whether NQO1 deficiency affects the autophagy process in response to cisplatin-induced nephrotoxicity. RESULTS: In vitro, NQO1 and autophagy-associated proteins were induced after cisplatin treatment and the autophagosomes markedly increased in the cisplatin-treated NQO1-knockdown ACHN cells together with increased ROS production...
May 20, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/26924060/autophagy-in-acute-kidney-injury
#17
REVIEW
Gur P Kaushal, Sudhir V Shah
Autophagy is a conserved multistep pathway that degrades and recycles damaged organelles and macromolecules to maintain intracellular homeostasis. The autophagy pathway is upregulated under stress conditions including cell starvation, hypoxia, nutrient and growth-factor deprivation, endoplasmic reticulum stress, and oxidant injury, most of which are involved in the pathogenesis of acute kidney injury (AKI). Recent studies demonstrate that basal autophagy in the kidney is vital for the normal homeostasis of the proximal tubules...
April 2016: Kidney International
https://www.readbyqxmd.com/read/26916346/autophagy-is-activated-to-protect-against-endotoxic-acute-kidney-injury
#18
Shuqin Mei, Man Livingston, Jielu Hao, Lin Li, Changlin Mei, Zheng Dong
Endotoxemia in sepsis, characterized by systemic inflammation, is a major cause of acute kidney injury (AKI) in hospitalized patients, especially in intensive care unit; however the underlying pathogenesis is poorly understood. Autophagy is a conserved, cellular catabolic pathway that plays crucial roles in cellular homeostasis including the maintenance of cellular function and viability. The regulation and role of autophagy in septic or endotoxic AKI remains unclear. Here we show that autophagy was induced in kidney tubular cells in mice by the endotoxin lipopolysaccharide (LPS)...
February 26, 2016: Scientific Reports
https://www.readbyqxmd.com/read/26907182/acute-renal-failure-in-transplanted-kidneys
#19
G Basta-Jovanovic, Lj Bogdanovic, M Radunovic, M Prostran, R Naumovic, S Simic-Ogrizovic, S Radojevic-Skodric
Free radical-mediated injury releases proinflammatory cytokines and activates innate immunity. It has been suggested that the early innate response and the ischemic tissue damage play roles in the development of adaptive responses, which may lead to acute kidney rejection. Various durations of hypothermic kidney storage before transplantation add to ischemic tissue damage. The final stage of ischemic injury occurs during reperfusion that develops hours or days after the initial insult. Repair and regeneration processes occur together with cellular apoptosis, autophagy and necrosis and a favorable outcome is expected if regeneration prevails...
February 24, 2016: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/26768243/acute-kidney-injury
#20
REVIEW
Anna Zuk, Joseph V Bonventre
Acute kidney injury (AKI) is a global public health concern associated with high morbidity, mortality, and healthcare costs. Other than dialysis, no therapeutic interventions reliably improve survival, limit injury, or speed recovery. Despite recognized shortcomings of in vivo animal models, the underlying pathophysiology of AKI and its consequence, chronic kidney disease (CKD), is rich with biological targets. We review recent findings relating to the renal vasculature and cellular stress responses, primarily the intersection of the unfolded protein response, mitochondrial dysfunction, autophagy, and the innate immune response...
2016: Annual Review of Medicine
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