Regulatory T Cells in AKI

Kinsey, Gilbert R.; Sharma, Rahul; Okusa, Mark D.

doi:10.1681/asn.2013050502

Cited by 84 publications

(69 citation statements)

References 68 publications

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“…Regulatory T cells produce multiple anti-inflammatory mediators, including IL-10, TGF-b1, and programmed cell death protein-1, which can counteract the effects of IR injury. 35,36 Furthermore, regulatory T cells express ectonucleoside triphosphate diphosphohydrolase (CD39) and ecto-59-nucleotidase (CD73), which convert proinflammatory ATP to cytoprotective adenosine. Enhanced adenosine generation in turn produces powerful anti-inflammatory effects via A 2a adenosine receptors.…”

Section: Volatile Anesthetics and Renal Protection Mechanismsmentioning

confidence: 99%

Volatile Anesthetics and AKI

Fukazawa

Lee

2014

Journal of the American Society of Nephrology

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AKI is a major clinical problem with extremely high mortality and morbidity. Kidney hypoxia or ischemia-reperfusion injury inevitably occurs during surgery involving renal or aortic vascular occlusion and is one of the leading causes of perioperative AKI. Despite the growing incidence and tremendous clinical and financial burden of AKI, there is currently no effective therapy for this condition. The pathophysiology of AKI is orchestrated by renal tubular and endothelial cell necrosis and apoptosis, leukocyte infiltration, and the production and release of proinflammatory cytokines and reactive oxygen species. Effective management strategies require multimodal inhibition of these injury processes. Despite the past theoretical concerns about the nephrotoxic effects of several clinically utilized volatile anesthetics, recent studies suggest that modern halogenated volatile anesthetics induce potent anti-inflammatory, antinecrotic, and antiapoptotic effects that protect against ischemic AKI. Therefore, the renal protective properties of volatile anesthetics may provide clinically useful therapeutic intervention to treat and/or prevent perioperative AKI. In this review, we outline the history of volatile anesthetics and their effect on kidney function, briefly review the studies on volatile anesthetic-induced renal protection, and summarize the basic cellular mechanisms of volatile anesthetic-mediated protection against ischemic AKI.

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Section: Volatile Anesthetics and Renal Protection Mechanismsmentioning

confidence: 99%

Volatile Anesthetics and AKI

Fukazawa

Lee

2014

Journal of the American Society of Nephrology

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“…Injury and death of tubular cells are especially recognized as the precipitating factors in AKI, and as an extension, tubular repair and regeneration are considered major events in kidney recovery from AKI. [5][6][7][8] Although sublethal injury is reversible, the death of tubular cells is accompanied by the inevitable loss of the function of the affected cells, and notably, it is also frequently the source of damageassociated molecular patterns (DAMPs), the stimulating and amplifying factors of inflammation in tissue damage. 9 In AKI, various forms of cell death are noticeable: necrosis and apoptosis.…”

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confidence: 99%

Regulated Cell Death in AKI

Linkermann

Chen

Dong

et al. 2014

Journal of the American Society of Nephrology

453

403

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AKI is pathologically characterized by sublethal and lethal damage of renal tubules. Under these conditions, renal tubular cell death may occur by regulated necrosis (RN) or apoptosis. In the last two decades, tubular apoptosis has been shown in preclinical models and some clinical samples from patients with AKI. Mechanistically, apoptotic cell death in AKI may result from well described extrinsic and intrinsic pathways as well as ER stress. Central converging nodes of these pathways are mitochondria, which become fragmented and sensitized to membrane permeabilization in response to cellular stress, resulting in the release of cell death-inducing factors. Whereas apoptosis is known to be regulated, tubular necrosis was thought to occur by accident until recent work unveiled several RN subroutines, most prominently receptorinteracting protein kinase-dependent necroptosis and RN induced by mitochondrial permeability transition. Additionally, other cell death pathways, like pyroptosis and ferroptosis, may also be of pathophysiologic relevance in AKI. Combination therapy targeting multiple cell-death pathways may, therefore, provide maximal therapeutic benefits.

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“…26 Therefore, we performed additional experiments to examine the ability of Tlr9 2/2 Tregs to undergo recruitment to the kidney. We previously observed fewer Tregs in kidneys of Tlr9 2/2 mice after cisplatin administration ( Figure 1D) Figure 4B).…”

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confidence: 99%