Autophagic cell death: Loch Ness monster or endangered species?

Shen, Han‐Ming; Codogno, Patrice

doi:10.4161/auto.7.5.14226

Cited by 296 publications

(253 citation statements)

References 99 publications

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“…Thus, autophagy could represent a failed adaptive mechanism that may have prevented death under milder conditions. Alternatively, excess activation of autophagy may contribute to cell death through unchecked degradative processes, however, the precise contribution of autophagy to cell death remains unclear (49,157). The terms ''autophagic cell death'' or type II programmed cell death have been used to refer to cell death distinct from apoptosis that occurs in association with increases in autophagosome formation, and independently of caspases (157).…”

Section: Autophagy At the Doorstep Of Cell Deathmentioning

confidence: 99%

“…The major features of apoptosis include nuclear degradation with chromosomal DNA fragmentation, cell surface blebbing, cell shrinkage, and mitochondrial dysfunction (48). Autophagy and apoptosis remain incompletely delineated, as the two processes are not always mutually exclusive and can simultaneously occur in the same cell (49,157). Suppression of autophagy by Beclin 1 or LC3 knockdown, or by chemical inhibitors such as 3-MA, can promote apoptosis and caspase-3 activation in starved HeLa cells.…”

Section: Autophagy At the Doorstep Of Cell Deathmentioning

confidence: 99%

“…Alternatively, excess activation of autophagy may contribute to cell death through unchecked degradative processes, however, the precise contribution of autophagy to cell death remains unclear (49,157). The terms ''autophagic cell death'' or type II programmed cell death have been used to refer to cell death distinct from apoptosis that occurs in association with increases in autophagosome formation, and independently of caspases (157). In contrast, apoptosis (type I programmed cell death) refers to a regulated form of cell death that requires proteases (e.g., caspases) and nucleases for cell death without loss of membrane integrity (48).…”

Section: Autophagy At the Doorstep Of Cell Deathmentioning

confidence: 99%

“…Autophagy influences several physiological and pathophysiological processes that may impact disease outcome. These include the regulation of mitochondrial homeostasis, as it relates to energy production and the execution of programmed cell death pathways (e.g., apoptosis) (48,49,157), and the regulation of innate or adaptive immune responses (36,95). This review will discuss the fundamental relationships between autophagy and cellular homeostasis, and its regulation by prooxidant states.…”

Section: Introductionmentioning

confidence: 99%

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Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

Nakahira

Cloonan

Mizumura

et al. 2014

Antioxidants & Redox Signaling

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Significance: Autophagy is a fundamental cellular process that functions in the turnover of subcellular organelles and protein. Activation of autophagy may represent a cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles. Selective forms of autophagy can maintain organelle populations or remove aggregated proteins. Autophagy can increase survival during nutrient deficiency and play a multifunctional role in host defense, by promoting pathogen clearance and modulating innate and adaptive immune responses. Recent Advances: Autophagy has been described as an inducible response to oxidative stress. Once believed to represent a random process, recent studies have defined selective mechanisms for cargo assimilation into autophagosomes. Such mechanisms may provide for protein aggregate detoxification and mitochondrial homeostasis during oxidative stress. Although long studied as a cellular phenomenon, recent advances implicate autophagy as a component of human diseases. Altered autophagy phenotypes have been observed in various human diseases, including lung diseases such as chronic obstructive lung disease, cystic fibrosis, pulmonary hypertension, and idiopathic pulmonary fibrosis. Critical Issues: Although autophagy can represent a pro-survival process, in particular, during nutrient starvation, its role in disease pathogenesis may be multifunctional and complex. The relationship of autophagy to programmed cell death pathways is incompletely defined and varies with model system. Future Directions: Activation or inhibition of autophagy may be used to alter the progression of human diseases. Further resolution of the mechanisms by which autophagy impacts the initiation and progression of diseases may lead to the development of therapeutics specifically targeting this pathway. Antioxid. Redox Signal. 20,

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Section: Autophagy At the Doorstep Of Cell Deathmentioning

confidence: 99%

Section: Autophagy At the Doorstep Of Cell Deathmentioning

confidence: 99%

Section: Autophagy At the Doorstep Of Cell Deathmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

Nakahira

Cloonan

Mizumura

et al. 2014

Antioxidants & Redox Signaling

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“…1 This process is enhanced under nutrient-limiting conditions to provide the needed nutrients for cell survival. [2][3][4] Given that intracellular components are broken down during this process, essential elements must be spared and the initiation and progression of autophagy must be tightly controlled, which is ensured by intricate regulatory mechanisms via numerous kinases and signaling pathways. One of the most pivotal groups of kinases controlling autophagy are the phosphatidylinositol 3-kinases (PtdIns3Ks) and the phosphoinositide 3-kinases (PI3Ks).…”

Section: Introductionmentioning

confidence: 99%

Differential regulatory functions of three classes of phosphatidylinositol and phosphoinositide 3-kinases in autophagy

2015

Self Cite

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Abbreviations: 3-MA, 3-methyladenine; AMBRA1, autophagy/Beclin 1 regulator 1; ATG, autophagy related; ATM, ATM serine/threonine kinase; ATR, ATR serine/threonine kinase; BH3, Bcl-2 homology 3; CCD, coiled-coil domain; CDK, cyclin-dependent kinase; CISD2, CDGSH iron sulfur domain 2; class I/II PI3K, class I/II phosphoinositide 3-kinase; class III PtdIns3K, class III phosphatidylinositol 3-kinase; DAPK1, death-associated protein kinase 1; DDR, DNA damage response; EIF4EBP1, eukaryotic translation initiation factor 4E binding protein 1; ER, endoplasmic reticulum; FOXO, forkhead box O; FYCO1, FYVE and coiledcoil domain containing 1; GAP, GTPase-activating protein; HMGB1, high mobility group box 1; HSPA1A, heat shock 70kDa protein 1A; IR, ionizing radiation; MAPK8, mitogen-activated protein kinase 8; MEFs, mouse embryonic fibroblasts; MTMR, myotubularin-related protein; MTOR, mechanistic target of rapamycin (serine/threonine kinase); MTORC1, mechanistic target of rapamycin complex 1; MVBs, spherical multivesicular bodies; NRBF2, nuclear receptor binding factor 2; PAS, phagophore assembly site; PDPK1, 3-phosphoinositide dependent protein kinase 1; PE, phosphatidylethanolamine; PIKFYVE, phosphoinositide kinase, FYVE finger containing; PINK1, PTEN-induced putative kinase 1; PtdIns3K-C1, class III phosphatidylinositol 3-kinase complex I; PtdIns3K-C2, class III phosphatidylinositol 3-kinase complex II; PKB, protein kinase B; PRKA, protein kinase, AMP-activated; PRKD1, protein kinase D1; PRKDC, protein kinase, DNA-activated, catalytic polypeptide; PtdIns5P, phosphatidylinositol 5-phosphate; PtdIns4P, phosphatidylinositol 4-phosphate; PtdIns(4,5)P 2 , phosphatidylinositol 4,5-bisphosphate; PtdIns3P, phosphatidylinositol 3-phosphate; PtdIns(3,5)P 2 , phosphatidylinositol 3,5-bisphosphate; PtdIns(3,4,5)P 3 , phosphatidylinositol 3,4,5-trisphosphate; RHEB, Ras homolog enriched in brain; RPS6KB1, ribosomal protein S6 kinase, 70kDa, polypeptide 1; SQSTM1, sequestosome 1; TECPR1, tectonin b-propeller repeat containing 1; TFEB, transcription factor EB; TRIM28, tripartite motif containing 28; TSC, tuberous sclerosis; UV, ultraviolet; UVRAG, UV radiation resistance associated; WDFY3, WD repeat and FYVE domain containing 3; WIPI, WD repeat domain, phosphoinositide interacting; ZFYVE1, zinc finger, FYVE domain containing 1.Autophagy is an evolutionarily conserved and exquisitely regulated self-eating cellular process with important biological functions. Phosphatidylinositol 3-kinases (PtdIns3Ks) and phosphoinositide 3-kinases (PI3Ks) are involved in the autophagic process. Here we aim to recapitulate how 3 classes of these lipid kinases differentially regulate autophagy. Generally, activation of the class I PI3K suppresses autophagy, via the well-established PI3K-AKT-MTOR (mechanistic target of rapamycin) complex 1 (MTORC1) pathway. In contrast, the class III PtdIns3K catalytic subunit PIK3C3/Vps34 forms a protein complex with BECN1 and PIK3R4 and produces phosphatidylinositol 3-phosphate (PtdIns3P), which is required for the initiati...

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Integration of Autophagy and Anoikis Resistance in Solid Tumors

Yang¹,

Zheng

Yan³

et al. 2013

The Anatomical Record

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Macroautophagy or autophagy is a lysosome-dependent process in which enzymatic degradation and recycling of cytosolic components occurred due to stressful conditions. This cellular arrangement imparts anoikis resistance in solid tumors. Anoikis, a special form of apoptosis occurring when cells detach from the extracellular matrix, is a critical mechanism in maintaining tissue homeostasis and development. Anoikis resistance facilitates tumorigenesis and metastasis. However, the complexity of the role of autophagy in tumor is underscored by evidence that autophagy can function as both a pro-survival or pro-death depending on the context and the stimuli, which are likely exploitable for tumor therapy. This review focuses on recent progress in understanding anoikis resistance and autophagy signaling, paying particular attention to its relevance in solid tumor metastasis. Anat Rec, 296:1501Rec, 296: -1508

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Autophagic cell death: Loch Ness monster or endangered species?

Cited by 296 publications

References 99 publications

Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

Differential regulatory functions of three classes of phosphatidylinositol and phosphoinositide 3-kinases in autophagy

Integration of Autophagy and Anoikis Resistance in Solid Tumors

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