MbrlCatalogueTitleDetail

Do you wish to reserve the book?
Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury
Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury
Hey, we have placed the reservation for you!
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury
Oops! Something went wrong.
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Title added to your shelf!
Title added to your shelf!
View what I already have on My Shelf.
Oops! Something went wrong.
Oops! Something went wrong.
While trying to add the title to your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury
Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury

Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
How would you like to get it?
We have requested the book for you! Sorry the robot delivery is not available at the moment
We have requested the book for you!
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury
Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury
Journal Article

Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury

2018
Request Book From Autostore and Choose the Collection Method
Overview
Platelet activation after muscle trauma promotes extracellular trap release by macrophages and acute kidney injury. Rhabdomyolysis is a serious syndrome caused by skeletal muscle injury and the subsequent release of breakdown products from damaged muscle cells into systemic circulation 1 . The muscle damage most often results from strenuous exercise, muscle hypoxia, medications, or drug abuse and can lead to life-threatening complications, such as acute kidney injury (AKI) 1 . Rhabdomyolysis and the AKI complication can also occur during crush syndrome, an emergency condition that commonly occurs in victims of natural disasters, such as earthquakes, and man-made disasters, such as wars and terrorism 2 . Myoglobin released from damaged muscle is believed to trigger renal dysfunction in this form of AKI. Recently, macrophages were implicated in the disease pathogenesis of rhabdomyolysis-induced AKI 3 , 4 , but the precise molecular mechanism remains unclear. In the present study, we show that macrophages released extracellular traps (ETs) comprising DNA fibers and granule proteins in a mouse model of rhabdomyolysis. Heme-activated platelets released from necrotic muscle cells during rhabdomyolysis enhanced the production of macrophage extracellular traps (METs) through increasing intracellular reactive oxygen species generation and histone citrullination. Here we report, for the first time to our knowledge, this unanticipated role for METs and platelets as a sensor of myoglobin-derived heme in rhabdomyolysis-induced AKI. This previously unknown mechanism might be targeted for treatment of the disease. Finally, we found a new therapeutic tool for prevention of AKI after rhabdomyolysis, which might rescue some sufferers of this pathology.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject

13

/ 13/1

/ 13/31

/ 14

/ 14/19

/ 38

/ 631/250/1932

/ 631/250/256/2516

/ 692/420/2780/262

/ 692/699/1585/4

/ 82

/ 82/51

/ 82/80

/ Acute kidney failure

/ Acute Kidney Injury - etiology

/ Acute Kidney Injury - genetics

/ Acute Kidney Injury - pathology

/ Animals

/ Biomedicine

/ Blood platelets

/ Cancer Research

/ Cell activation

/ Cellular biology

/ Citrullination - genetics

/ Citrulline

/ Complications and side effects

/ Crush Syndrome - etiology

/ Crush Syndrome - genetics

/ Crush Syndrome - pathology

/ Damage

/ Deoxyribonucleic acid

/ Development and progression

/ Disease Models, Animal

/ DNA

/ DNA - genetics

/ DNA - metabolism

/ Drug abuse

/ Earthquakes

/ Extracellular Traps - genetics

/ Extracellular Traps - metabolism

/ Fibers

/ Genetic aspects

/ Heme

/ Heme - metabolism

/ Histones - metabolism

/ Humans

/ Hypoxia

/ Infectious Diseases

/ Injuries

/ Kidneys

/ letter

/ Macrophages

/ Macrophages - metabolism

/ Macrophages - pathology

/ Man made disasters

/ Metabolic Diseases

/ Mice

/ Molecular Medicine

/ Muscle, Skeletal - injuries

/ Muscle, Skeletal - pathology

/ Muscles

/ Myoglobin - genetics

/ Myoglobins

/ Natural disasters

/ Neurosciences

/ Pathogenesis

/ Physiological aspects

/ Platelet Activation - genetics

/ Platelets

/ Proteins

/ Reactive oxygen species

/ Reactive Oxygen Species - metabolism

/ Renal function

/ Rhabdomyolysis

/ Rhabdomyolysis - complications

/ Rhabdomyolysis - genetics

/ Rhabdomyolysis - pathology

/ Rodents

/ Secretory Vesicles - genetics

/ Seismic activity

/ Skeletal muscle

/ Terrorism