https://hull-repository.worktribe.com/preview/1797952/1-s2.0-S0140673618322797-main.pdf

Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016

https://openresearch-repository.anu.edu.au/bitstream/1885/164632/2/01_Bin%2bSayeed_Global%252C_regional%252C_and_national_2018.pdf

Global, regional, and national incidence, prevalence, andyears lived with disability for 354 diseases and injuries for195 countries and territories, 1990–2017: a systematicanalysis for the Global Burden of Disease Study 2017

WRITING GROUP MEMBERS Emelia J. Benjamin, MD, SCM, FAHA Michael J. Blaha, MD, MPH Stephanie E. Chiuve, ScD Mary Cushman, MD, MSc, FAHA Sandeep R. Das, MD, MPH, FAHA Rajat Deo, MD, MTR Sarah D. de Ferranti, MD, MPH James Floyd, MD, MS Myriam Fornage, PhD, FAHA Cathleen Gillespie, MS Carmen R. Isasi, MD, PhD, FAHA Monik C. Jiménez, ScD, SM Lori Chaffin Jordan, MD, PhD Suzanne E. Judd, PhD Daniel Lackland, DrPH, FAHA Judith H. Lichtman, PhD, MPH, FAHA Lynda Lisabeth, PhD, MPH, FAHA Simin Liu, MD, ScD, FAHA Chris T. Longenecker, MD Rachel H. Mackey, PhD, MPH, FAHA Kunihiro Matsushita, MD, PhD, FAHA Dariush Mozaffarian, MD, DrPH, FAHA Michael E. Mussolino, PhD, FAHA Khurram Nasir, MD, MPH, FAHA Robert W. Neumar, MD, PhD, FAHA Latha Palaniappan, MD, MS, FAHA Dilip K. Pandey, MBBS, MS, PhD, FAHA Ravi R. Thiagarajan, MD, MPH Mathew J. Reeves, PhD Matthew Ritchey, PT, DPT, OCS, MPH Carlos J. Rodriguez, MD, MPH, FAHA Gregory A. Roth, MD, MPH Wayne D. Rosamond, PhD, FAHA Comilla Sasson, MD, PhD, FAHA Amytis Towfighi, MD Connie W. Tsao, MD, MPH Melanie B. Turner, MPH Salim S. Virani, MD, PhD, FAHA Jenifer H. Voeks, PhD Joshua Z. Willey, MD, MS John T. Wilkins, MD Jason HY. Wu, MSc, PhD, FAHA Heather M. Alger, PhD Sally S. Wong, PhD, RD, CDN, FAHA Paul Muntner, PhD, MHSc On behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart Disease and Stroke Statistics—2017 Update

Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association

The last decade has seen a sharp increase in the number of scientific publications describing physiological and pathological functions of extracellular vesicles (EVs), a collective term covering various subtypes of cell-released, membranous structures, called exosomes, microvesicles, microparticles, ectosomes, oncosomes, apoptotic bodies, and many other names. However, specific issues arise when working with these entities, whose size and amount often make them difficult to obtain as relatively pure preparations, and to characterize properly. The International Society for Extracellular Vesicles (ISEV) proposed Minimal Information for Studies of Extracellular Vesicles (“MISEV”) guidelines for the field in 2014. We now update these “MISEV2014” guidelines based on evolution of the collective knowledge in the last four years. An important point to consider is that ascribing a specific function to EVs in general, or to subtypes of EVs, requires reporting of specific information beyond mere description of function in a crude, potentially contaminated, and heterogeneous preparation. For example, claims that exosomes are endowed with exquisite and specific activities remain difficult to support experimentally, given our still limited knowledge of their specific molecular machineries of biogenesis and release, as compared with other biophysically similar EVs. The MISEV2018 guidelines include tables and outlines of suggested protocols and steps to follow to document specific EV-associated functional activities. Finally, a checklist is provided with summaries of key points.

/pdf/minimal-information-for-studies-of-extracellular-vesicles-3s0intarv4.pdf

Minimal information for studies of extracellular vesicles 2018 (MISEV2018) : a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines

https://research-information.bris.ac.uk/ws/files/259213304/PIIS0140673620309259.pdf

Global burden of 369 diseases and injuries in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Disorders of cell number that result from an imbalance between the death of parenchymal cells and the proliferation or recruitment of maladaptive cells contributes to the pathogenesis of kidney disease. Acute kidney injury can result from an acute loss of kidney epithelial cells. In chronic kidney disease, loss of kidney epithelial cells leads to glomerulosclerosis and tubular atrophy, whereas interstitial inflammation and fibrosis result from an excess of leukocytes and myofibroblasts. Other conditions, such as acquired cystic disease and kidney cancer, are characterized by excess numbers of cyst wall and malignant cells, respectively. Cell death modalities act to clear unwanted cells, but disproportionate responses can contribute to the detrimental loss of kidney cells. Indeed, pathways of regulated cell death - including apoptosis and necrosis - have emerged as central events in the pathogenesis of various kidney diseases that may be amenable to therapeutic intervention. Modes of regulated necrosis, such as ferroptosis, necroptosis and pyroptosis may cause kidney injury directly or through the recruitment of immune cells and stimulation of inflammatory responses. Importantly, multiple layers of interconnections exist between different modalities of regulated cell death, including shared triggers, molecular components and protective mechanisms. 

/pdf/regulated-cell-death-pathways-in-kidney-disease-2ko2ukv2.pdf

Regulated cell death pathways in kidney disease

Sodium-glucose co-transporter-2 inhibitors increase Klotho in patients with diabetic kidney disease: A clinical and experimental study.

Since the seminal observation that high glucose induces renal cell apoptosis in culture and in vivo ,1 investigators have sought to identify the molecular mechanisms of renal cell apoptosis in diabetic nephropathy. In this issue of JASN , Brezniceanu et al. 2 explore proapoptotic genes that are upregulated differentially by reactive oxygen species (ROS) in renal proximal tubular cells of diabetic (db/db) mice. Expression of caspase-12 and other endoplasmic reticulum (ER) stress genes, such as HSPA5/GRP78/BiP and CHOP, are increased in the proximal tubules of these mice compared with nondiabetic and diabetic catalase transgenic mice. Reduction of ROS generation also inhibits albumin-stimulated expression and activity of caspase-12 in a human proximal tubule cell line (HK-2). Furthermore, knockdown of caspase-12 with small interfering RNAs reduces albumin-induced apoptosis in HK-2 cells. The authors of this article conclude that albuminuria may induce ROS-mediated ER stress and subsequent tubular apoptosis in diabetic kidneys. The involvement of caspase-12 in this process, especially in human cells, stands out as the most original part of the article; however, no information is provided on human diabetic nephropathy, and the key question is how relevant these data are to humans.

There is increasing evidence that renal cells, including tubular cells, are lost through apoptosis in experimental and human diabetic nephropathy. Recent efforts to identify novel changes …

Caspase-12 and diabetic nephropathy: from mice to men?

El articulo original ha sido publicado: Jankowski V, Tolle M, Tran TNA, van der Giet M, Schuchardt M, et al. (2013) Identification of a Potent Endothelium-Derived Angiogenic Factor. PLoS ONE 8(7): e68575. doi:10.1371/journal.pone.0068575

Correction: Identification of a Potent Endothelium-Derived Angiogenic Factor

ABSTRACT Diet has long been known to influence the course of chronic kidney disease (CKD) and may even result in acute kidney injury (AKI). Diet may influence kidney disease through a direct impact of specific nutrients on the human body through modulation of the gut microbiota composition or through metabolites generated by the gut microbiota from ingested nutrients. The potential for interaction between diet, microbiota and CKD has fueled research into interventions aimed at modifying the microbiota to treat CKD. These interventions may include diet, probiotics, prebiotics, fecal microbiota transplant and other interventions that modulate the microbiota and its metabolome. A recent report identified Lactobacillus casei Zhang from traditional Chinese koumiss as a probiotic that may protect mice from AKI and CKD and slow CKD progression in humans. Potential mechanisms of action include modulation of the gut microbiota and increased availability of short-chain fatty acids with anti-inflammatory properties and of nicotinamide. However, the clinical relevance needs validation in large well-designed clinical trials.

/pdf/probiotics-for-kidney-disease-1kv6n7ai.pdf

Maria Dolores Sanchez-Niño

Papers

Regulated cell death pathways in kidney disease

Sodium-glucose co-transporter-2 inhibitors increase Klotho in patients with diabetic kidney disease: A clinical and experimental study.

Caspase-12 and diabetic nephropathy: from mice to men?

Correction: Identification of a Potent Endothelium-Derived Angiogenic Factor

Probiotics for kidney disease