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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Am+Soc+Nephrol
2014 ; 25
(12
): 2689-701
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Regulated cell death in AKI
#MMPMID24925726
Linkermann A
; Chen G
; Dong G
; Kunzendorf U
; Krautwald S
; Dong Z
J Am Soc Nephrol
2014[Dec]; 25
(12
): 2689-701
PMID24925726
show ga
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 receptor-interacting 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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