Nature Immunology, Journal Year: 2012, Volume and Issue: 13(4), P. 343 - 351
Published: March 18, 2012
Language: Английский
Nature Immunology, Journal Year: 2012, Volume and Issue: 13(4), P. 343 - 351
Published: March 18, 2012
Language: Английский
Cell, Journal Year: 2013, Volume and Issue: 153(6), P. 1194 - 1217
Published: June 1, 2013
Language: Английский
Citations
12714Cell Death and Differentiation, Journal Year: 2018, Volume and Issue: 25(3), P. 486 - 541
Published: Jan. 23, 2018
Over the past decade, Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for definition and interpretation of cell death from morphological, biochemical, functional perspectives. Since field continues to expand novel mechanisms that orchestrate multiple pathways are unveiled, we propose an updated classification subroutines focusing mechanistic essential (as opposed correlative dispensable) aspects process. As provide molecularly oriented definitions terms including intrinsic apoptosis, extrinsic mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic death, NETotic lysosome-dependent autophagy-dependent immunogenic cellular senescence, mitotic catastrophe, discuss utility neologisms refer highly specialized instances these processes. The mission NCCD is a widely accepted nomenclature in support continued development field.
Language: Английский
Citations
5351Cell Metabolism, Journal Year: 2015, Volume and Issue: 21(6), P. 805 - 821
Published: June 1, 2015
Language: Английский
Citations
1152The EMBO Journal, Journal Year: 2015, Volume and Issue: 34(7), P. 856 - 880
Published: Feb. 23, 2015
Language: Английский
Citations
1089Frontiers in Immunology, Journal Year: 2018, Volume and Issue: 9
Published: April 9, 2018
Cytokine dysregulation is believed to play a key role in the remodeling of immune system at older age, with evidence pointing an inability fine-control systemic inflammation, which seems be marker unsuccessful aging. This reshaping cytokine expression pattern, progressive tendency toward pro-inflammatory phenotype has been called 'inflamm-aging'. Despite research there no clear understanding about causes 'inflamm-aging' that underpin most major age-related diseases including atherosclerosis, diabetes, Alzheimer's disease, rheumatoid arthritis, cancer and aging itself. While inflammation part normal repair response for healing, essential keeping us safe from bacterial viral infections noxious environmental agents, not all good. When becomes prolonged persists, it can become damaging destructive. Several common molecular pathways have identified are associated both low-grade inflammation. The change redox balance, increase senescent cells SASP decline effective autophagy trigger inflammasome, suggest may possible delay itself by suppressing mechanisms or improving timely resolution Conversely learning genetic long-lived cohorts who exemplify good quality Here we will discuss some current ideas highlight appear contribute imbalance dysregulation, 'inflammageing' parainflammation. Evidence these findings drawn cardiovascular disease two
Language: Английский
Citations
1045Biological Chemistry, Journal Year: 2012, Volume and Issue: 393(7), P. 547 - 564
Published: July 1, 2012
Abstract Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death. The removal of damaged mitochondria through autophagy, a process called mitophagy, is thus critical for maintaining proper functions. Indeed, mitophagy has been recently proposed to play roles in terminal differentiation red blood cells, paternal mitochondrial degradation, neurodegenerative diseases, ischemia or drug-induced tissue injury. Removal autophagy requires two steps: induction general priming selective autophagic recognition. Recent progress studies reveals mediated either by the Pink1-Parkin signaling pathway mitophagic receptors Nix Bnip3. In this review, we summarize our current knowledge on mechanisms mitophagy. We also discuss pathophysiological assays used monitor
Language: Английский
Citations
914Journal of Hepatology, Journal Year: 2013, Volume and Issue: 59(3), P. 583 - 594
Published: April 6, 2013
Inflammation can be either beneficial or detrimental to the liver, depending on multiple factors. Mild (i.e., limited in intensity and destined resolve) inflammatory responses have indeed been shown exert consistent hepatoprotective effects, contributing tissue repair promoting re-establishment of homeostasis. Conversely, excessive disproportionate permanent) inflammation may induce a massive loss hepatocytes hence exacerbate severity various hepatic conditions, including ischemia-reperfusion injury, systemic metabolic alterations (e.g., obesity, diabetes, non-alcoholic fatty liver disorders), alcoholic hepatitis, intoxication by xenobiotics infection, de facto being associated with irreversible damage, fibrosis, carcinogenesis. Both liver-resident cells Kupffer cells, stellate sinusoidal endothelial cells) that are recruited response injury monocytes, macrophages, dendritic natural killer emit pro-inflammatory signals – but not cytokines, chemokines, lipid messengers, reactive oxygen species contribute apoptotic necrotic demise hepatocytes. In turn, dying release damage-associated molecular patterns that-upon binding evolutionary conserved pattern recognition receptors-activate innate immune system further stimulate responses, establishing highly hepatotoxic feedforward cycle cell death. this review, we discuss cellular mechanisms account for most deleterious effect at level, is, initiation death among
Language: Английский
Citations
881Cell, Journal Year: 2014, Volume and Issue: 159(6), P. 1263 - 1276
Published: Dec. 1, 2014
Language: Английский
Citations
771Chemical Society Reviews, Journal Year: 2017, Volume and Issue: 46(8), P. 2237 - 2271
Published: Jan. 1, 2017
This review focuses on small molecular ligand-targeted fluorescent imaging probes and theranostics, including their design strategies applications in clinical tumor treatment.
Language: Английский
Citations
750Nature Reviews Drug Discovery, Journal Year: 2017, Volume and Issue: 16(7), P. 487 - 511
Published: May 19, 2017
Language: Английский
Citations
749