scholarly journals Molecular Circuits of Resolution in Renal Disease

2010 ◽  
Vol 10 ◽  
pp. 1370-1385 ◽  
Author(s):  
Emma Börgeson ◽  
Catherine Godson

Inflammation is a common feature of renal pathology. Lipid mediators, such as lipoxins, resolvins, and protectins, can actively promote the resolution of inflammation by inhibiting polymorphonuclear cell infiltration to the site of inflammation, shifting the cytokine milieu from proinflammatory to proresolving and increasing the nonphlogistic phagocytosis of apoptotic cells by macrophages. Here we review the evidence for molecular circuits of resolution in renal disease.

2020 ◽  
Vol 21 (18) ◽  
pp. 6637 ◽  
Author(s):  
Antonio Recchiuti ◽  
Elisa Isopi ◽  
Mario Romano ◽  
Domenico Mattoscio

Autophagy is a catabolic pathway that accounts for degradation and recycling of cellular components to extend cell survival under stress conditions. In addition to this prominent role, recent evidence indicates that autophagy is crucially involved in the regulation of the inflammatory response, a tightly controlled process aimed at clearing the inflammatory stimulus and restoring tissue homeostasis. To be efficient and beneficial to the host, inflammation should be controlled by a resolution program, since uncontrolled inflammation is the underlying cause of many pathologies. Resolution of inflammation is an active process mediated by a variety of mediators, including the so-called specialized pro-resolving lipid mediators (SPMs), a family of endogenous lipid autacoids known to regulate leukocyte infiltration and activities, and counterbalance cytokine production. Recently, regulation of autophagic mechanisms by these mediators has emerged, uncovering unappreciated connections between inflammation resolution and autophagy. Here, we summarize mechanisms of autophagy and resolution, focusing on the contribution of autophagy in sustaining paradigmatic examples of chronic inflammatory disorders. Then, we discuss the evidence that SPMs can restore dysregulated autophagy, hypothesizing that resolution of inflammation could represent an innovative approach to modulate autophagy and its impact on the inflammatory response.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Dimitra Vasileia Daikidou ◽  
MARIA STANGOU ◽  
Erasmia Sampani ◽  
Despoina Asouchidou ◽  
Vasiliki Nikolaidou ◽  
...  

Abstract Background and Aims Lymphocyte apoptosis, as a programmed mechanism of lymphocyte death, is essential in maintaining homeostasis and balance between inflammatory and immune reactions. Disturbances in the apoptotic progress, leading to fragmented lymphocytes, “late apoptotic” cells, may result in immunodeficiency, oncogenesis, atheromatosis, etc. Aim of the present study was to investigate the lymphocyte apoptotic progress in End Stage Renal Disease (ESRD) and the effect of dialysis. Method The study included patients on ESRD; measurements were performed at the first day of dialysis (T0) and repeated 6 months later (T6), while being on dialysis. Total lymphocytes and B lymphocytes (CD19+) were gated and stained with Annexin V to detect apoptotic cells; early and late apoptotic cells were quantified. The results were compared to age-matched healthy control group. Results ESRD patients had reduced lymphocyte and B cell count, 1550±592μ/L vs. 2692±690μ/L, p<0.001 and 120.4±80μ/L vs. 321.7±184.7μ/L, p=0.002, respectively, compared to controls. There was an increase in total lymphocytes and B cells, being on later apoptotic stages (LAS) in ESRD-T0 compared to controls, 0.3±0.8% vs. 0.06±0.1%, and 0.04±0.08% vs. 0.01±0.03%, respectively, although differences did not reach statistical significance. After 6 months on dialysis, a reduction was noticed in the population of lymphocytes on LAS, 0.18±0.2% from 0.34±0.8%, while there was an increase of B cells on LAS, 0.1±0.2% from 0.02±0.07, with subsequent alterations in total numbers of apoptotic cells were also evident Conclusion Late apoptotic changes affecting total and particularly B lymphocytes happen in ESRD, and initiation of dialysis seem to cause further alterations, which may be implicated in the increased morbidity and mortality of disease


1990 ◽  
Vol 55 (3) ◽  
pp. 907-912 ◽  
Author(s):  
Jian Xu ◽  
Chung Y. Hsu ◽  
Tsung H. Liu ◽  
Edward L. Hogan ◽  
Phanor L. Perot ◽  
...  

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Wim Laurens ◽  
Johan De Meester ◽  
Ben Sprangers ◽  
Steven Van Laecke ◽  
Dendooven Amélie ◽  
...  

Abstract Background and Aims End December 2016, a renal biopsy network in the Flemish region (Belgium) was founded as a collaboration between the renal pathologists and nephrologists. This FCGG network introduced a uniform renal biopsy request form, a well-structured report form of the renal pathology examination and a comprehensive list of renal pathology diagnoses. Method Following informed consent [99.5%] and in compliance with GDPR, the registration of the renal biopsies consists of basic categorical renal data, structured renal pathology information and the final clinical renal disease. Results In 2017 and 2018, 1385 renal biopsies were registered – 10.5 per million inhabitants per year; in addition, 28 patients had a repeat biopsy in the same time frame (2%). Of the pediatric patients ( age < 18 years; N=92; 6.6%), 23 had IgA nephropathy, 20 a minimal change disease and 15 another type of glomerulonephritis. The biopsy was reported as normal or non-diagnostic in 15 patients (16%) – the majority was clinically considered as glomerulonephritis. The spectrum of the adult population was quite similar across gender and age groups: 56% glomerulonephritis [= IgA nephropathy [19%] + FSGS [8%] + pauci-immune glomerulonephritis [7%] + other GN [22%] ), 10% tubulo-interstitial nephritis, 7% acute tubular necrosis [ATN], 7% diabetes mellitus, and 7% nephroangiosclerosis. Exceptions are pauci-immune glomerulonephritis as the most important renal disease in women aged 65 years and older, and lupus nephritis as the second most important glomerulonephritis in women aged 18-44 years. Only a small percentage of adult renal biopsies yielded no result (7%), clinically interpreted as glomerulonephritis in 50% of the cases. Conclusion The FCGG network has provided a more intense collaboration between renal pathologists and nephrologists mainly by standardizing the renal biopsy reading and reporting across all centers. More precise estimates of the prevalent renal diseases were provided for the first time; however, in order to get full information, renal diseases diagnosed by other techniques ( serology, genetic analysis ) should also be collected in the future. Efforts will be done to coordinate the clinical care of renal diseases, particularly the more rare renal diseases, and to offer access to new therapeutic molecules or new schemes, through this super-regional network.


2007 ◽  
Vol 35 (2) ◽  
pp. 288-291 ◽  
Author(s):  
A.G. Rossi ◽  
J.M. Hallett ◽  
D.A. Sawatzky ◽  
M.M. Teixeira ◽  
C. Haslett

Apoptosis of granulocytes and the subsequent clearance of apoptotic cells are important processes for the successful resolution of inflammation. Signalling pathways, including those involving NF-κB (nuclear factor κB), MAPK (mitogen-activated protein kinase) and PI3K (phosphoinositide 3-kinase) have been shown to be key regulators of inflammatory cell survival and apoptosis in vitro. In addition, manipulation of such pathways in vivo has indicated that they also play a role in the resolution of inflammation. Furthermore, manipulation of proteins directly involved in the control of apoptosis, such as Bcl-2 family members and caspases, can be targeted in vivo to influence inflammatory resolution. Recently, it has been shown that CDK (cyclin-dependent kinase) inhibitor drugs induce caspase-dependent human neutrophil apoptosis possibly by altering levels of the anti-apoptotic Bcl-2 family member, Mcl-1. Importantly, CDK inhibitor drugs augment the resolution of established ‘neutrophil-dominant’ inflammation by promoting apoptosis of neutrophils. Thus manipulation of apoptotic pathways, together with ensuring macrophage clearance of apoptotic cells, appears to be a viable pharmacological target for reducing established inflammation.


2009 ◽  
Vol 390 (5/6) ◽  
Author(s):  
Andreas Weigert ◽  
Carla Jennewein ◽  
Bernhard Brüne

AbstractThe efficient execution of apoptotic cell death with the clearance of apoptotic debris by phagocytes is a key regulatory mechanism ensuring tissue homeostasis. Failure in this execution program contributes to the pathogenesis of many human diseases. In this review, we describe the current knowledge regarding the interaction of apoptotic cells with their professional ‘captors’, the macrophages, with special emphasis on the immunological outcome. Removal of apoptotic cells must be considered as a process that actively delivers signals to polarize macrophages, which are fundamental for the resolution of inflammation. However, the sculpting of macrophage responses by apoptotic cells can be misused under certain inflammatory disease conditions, including tumor development.


Spinal Cord ◽  
1984 ◽  
Vol 22 (1) ◽  
pp. 31-41 ◽  
Author(s):  
C H Barton ◽  
N D Vaziri ◽  
S Gordon ◽  
S Tilles

2018 ◽  
Vol 315 (6) ◽  
pp. F1652-F1655
Author(s):  
Serena M. Bagnasco

As rapid progress in science and biotechnology is affecting the practice of renal medicine, increasingly precise diagnostic assessment is needed to select the most effective therapeutic approach for individual patients. The kidney biopsy remains the gold standard for the diagnosis of renal disease, but the field of renal pathology is evolving, classification of renal parenchyma lesions and histopathological diagnostic criteria are undergoing more validation and updates, and new technologies and assays are sought to improve efficiency and accuracy of the diagnostic process. How new knowledge and scientific advances may potentially affect renal pathology is discussed.


2002 ◽  
Vol 2 (10) ◽  
pp. 787-795 ◽  
Author(s):  
Toby Lawrence ◽  
Derek A. Willoughby ◽  
Derek W. Gilroy

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