Necrotic death as a cell fate.

By W. Zong, Craig B. Thompson. Genes & Development, 2006

988 citations recorded by the source corpus.

Organismal homeostasis depends on an intricate balance between cell death and renewal. Early pathologists recognized that this balance could be disrupted by the extensive damage observed in internal organs during the course of certain diseases. This form of tissue damage was termed "necrosis", derived from the Greek "nekros" for corpse. As it became clear that the essential building block of tissue was the cell, necrosis came to be used to describe pathologic cell death. Until recently, necrotic cell death was believed to result from injuries that caused an irreversible bioenergetic compromise. The cell dying by necrosis has been viewed as a victim of extrinsic events beyond its control. However, recent evidence suggests that a cell can initiate its own demise by necrosis in a manner that initiates both inflammatory and/or reparative responses in the host. By initiating these adaptive responses, programmed cell necrosis may serve to maintain tissue and organismal integrity.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/81f35eb022ed98e7b7c1efb193f39d6e2547abe2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Physiology

Citations in the corpus

Hallmarks of cancer: the next generation. (2011, positive): “Although necrosis has historically been viewed much like organismic death, as a form of system-wide exhaustion and breakdown, the conceptual landscape is changing: cell death by necrosis is clearly under genetic control in some circumstances, rather than being a random and undirected process (Galluz”
Role of autophagy in cancer (2007, background): “Although diverting apoptosis-defective tumour cells to a necrotic cell fate may not be a benign cell deat”
NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, neutral): “mediator of programmed necrosis (350, 351), there have been”
p53 opens the mitochondrial permeability transition pore to trigger necrosis (2012, background): “Rather than being a passive event, necrosis has emerged as a controlled cell death that induces an inflammatory response to stimulate tissue repair by selectively releasing factors like HMGB1 and HDGF from dying cells (Zong and Thompson, 2006).”
Crosstalk between apoptosis, necrosis and autophagy. (2013, background): “Necrotic cells selectively release factors like HMGB1 and HDGF to evoke an in ﬂ ammatory response [8] and are sensed by NLRP3, a core protein of the in ﬂ ammasome, resulting in in ﬂ ammasome activation and the subsequent release of the pro-in ﬂ ammatory cytokine IL1 β .”
Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. (2006, background): “A third means to achieve cell death is by necrosis, which usually is associated with physical insults, failure of osmotic regulation, ATP depletion, HMGB1 release, cell lysis, and an inflammatory response that may facilitate wound healing (Kanduc et al., 2002; Majno and Joris, 1995; Nelson and White”
Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “Because inhibition of ceramide accumulation clearly diminished caspase-independent PCD but not as completely as inhibition of RIP1, ceramide obviously represents a central factor, but most likely not the only one, transmitting the death signals generated by RIP1 in response to TNFα.”
Induction of autophagy by spermidine promotes longevity (2009, background): “Recent research suggests, however, that the occurrence and course of necrosis can be subject to complex controlled processes and that necrosis can therefore also be 'programmed”
PHOTODYNAMIC THERAPY OF CANCER: AN UPDATE (2011, background): “necrosis are still elusive, but certain events including activation of receptor interacting protein 1 (RIP1) kinase, excessive mitochondrial ROS production, lysosomal damage, and intracellular Ca2þ overload are recurrently involved.(33,34) Severe inner mitochondria membrane photodamage or intracellu”
Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “Until recently, necrosis was thought to be an unregulated process, but recent studies suggest that necrosis can be regulated and that interventions can reduce necrotic cell death (83, 290).”
Immunity, Inflammation, and Cancer (2010, neutral): “Radiation and chemotherapy cause massive necrotic death of cancer cells and surrounding tissues, which in turn trigger an inflammatory reaction analogous to a wound-healing response (Zong and Thompson, 2006).”