scholarly journals 097 An important role of TRPV3 in the temporal control of intracellular acidification in corneoptosis, a unique cell death process of keratinocytes

2021 ◽  
Vol 141 (10) ◽  
pp. S165
Author(s):  
T. Matsui ◽  
N. Kadono-Maekubo ◽  
Y. Suzuki ◽  
Y. Furuichi ◽  
K. Shiraga ◽  
...  
Keyword(s):  
Cell Death ◽  
Death Process ◽  
Temporal Control ◽  
Intracellular Acidification ◽  
Cell Death Process ◽  
Unique Cell

scholarly journals Ferroptosis and its facet in Cancer therapy

2021 ◽  
Vol 6 (1) ◽  
pp. 10-15
Author(s):  
Shreya Shreshtha
Keyword(s):  
Cell Death ◽  
Cell Therapy ◽  
Cancer Cell ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Death Process ◽  
Cell Organelles ◽  
Clinical Role ◽  
Cell Death Process

Ferroptosis is a regulated process impelled by iron-dependent lipid peroxidation. It is a new type of cell destruction processes including apoptosis, autophagy and necrosis. It demonstrates mainly the contraction of mitochondria and expansion of mitochondrial membrane density which does not lead to any alteration in morphology. Due to the malfunctioning of ferroptosis several disorders arise which includes damage of one or more nerve which leads to numbness and muscle weakness whereas ischemia reperfusion injury, acute kidney failure and cancer also occurs. Also, ferroptosis is induced in large number of cancer cells through series of small molecules which helps in to bringing out this process. In scientific research and medicine many findings contribute in the chance of defeating cancer by genetic or pharmacological interference with ferroptosis cell death which is appealing for various researches. There are multiple pathways and cell organelles which plays a role in ferroptosis regulation. Ongoing studies on ferroptosis have demonstrated its role in humans though its mechanism is not yet clear. Recently, various studies have encouraged the role of this newly emerged cell death process and also showed some effective usage in the treatment of cancer. Here, we review the mitochondrial aspect of ferroptosis as well as discuss on the role of ferroptosis in Cancer cell therapy. We will also aim on the future scope of ferroptosis in the treatment of Cancer as well as discuss about the problems related to its clinical role which may trigger the cancer cell therapy.

Understanding the role of Inflammasome in Angina Pectoris

2020 ◽  
Vol 21 ◽  
Author(s):  
Ishita Sharma ◽  
Tapan Behl ◽  
Simona Bungau ◽  
Monika Sachdeva ◽  
Arun Kumar ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Angina Pectoris ◽  
Nlrp3 Inflammasome ◽  
Vital Role ◽  
Death Process ◽  
Cell Death Process ◽  
Artery Disease ◽  
Species Production ◽  
Pro Inflammatory Cytokines

Abstract:: Angina pectoris, associated with coronary artery disease, a cardiovascular disease where, pain is caused by adverse oxygen supply in myocardium, resulting in contractility and discomfort in chest. Inflammasomes, triggered by stimuli due to infection and cellular stress have identified to play a vital role in the progression of cardiovascular disorders and thus, causing various symptoms like angina pectoris. Nlrp3 inflammasome, a key contributor in the pathogenesis of angina pectoris, requires activation and primary signaling for the commencement of inflammation. Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Thus, inflammasome are considered to be one of the factors involved in the progression of coronary artery diseases and have an intricate role in development of angina pectoris.

scholarly journals Correction: PML induces a novel caspase-independent cell death process

10.1038/8706 ◽  
1999 ◽  
Vol 22 (1) ◽  
pp. 115-115 ◽  
Author(s):  
Fredérique Quignon
Keyword(s):  
Cell Death ◽  
Death Process ◽  
Cell Death Process

scholarly journals Production of Prodiginines Is Part of a Programmed Cell Death Process in Streptomyces coelicolor

2018 ◽  
Vol 9 ◽  
Author(s):  
Elodie Tenconi ◽  
Matthew F. Traxler ◽  
Charline Hoebreck ◽  
Gilles P. van Wezel ◽  
Sébastien Rigali
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Streptomyces Coelicolor ◽  
Death Process ◽  
Cell Death Process

Characterization of cell death process in plant cells induced by hipoxia and anoxia

2000 ◽  
Vol 28 (5) ◽  
pp. A372-A372
Author(s):  
E. N. Baranova ◽  
N. V. Kononenko ◽  
T. V. Bragina ◽  
G. M. Grineva ◽  
T. P. Astafurova ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Cells ◽  
Death Process ◽  
Cell Death Process

Internucleosomal DNA fragmentation and programmed cell death (apoptosis) in the interdigital tissue of the embryonic chick leg bud

1993 ◽  
Vol 106 (1) ◽  
pp. 201-208 ◽  
Author(s):  
V. Garcia-Martinez ◽  
D. Macias ◽  
Y. Ganan ◽  
J.M. Garcia-Lobo ◽  
M.V. Francia ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Limb Development ◽  
Light Transmission ◽  
Morphological Changes ◽  
Death Process ◽  
Chondrogenic Potential ◽  
Cell Death Process ◽  
Dying Cells

In this work we have attempted to characterize the programmed cell death process in the chick embryonic interdigital tissue. Interdigital cell death is a prominent phenomenon during limb development and has the role of sculpturing the digits. Morphological changes in the regressing interdigital tissue studied by light, transmission and scanning electron microscopy were correlated with the occurrence of internucleosomal DNA fragmentation, evaluated using agarose gels. Programming of the cell death process was also analyzed by testing the chondrogenic potential of the interdigital mesenchyme, in high density cultures. Our results reveal a progressive loss of the chondrogenic potential of the interdigital mesenchyme, detectable 36 hours before the onset of the degenerative process. Internucleosomal DNA fragmentation was only detected concomitant with the appearance of cells dying with the morphology of apoptosis, but unspecific DNA fragmentation was also present at the same time. This unspecific DNA fragmentation was explained by a precocious activation of the phagocytic removal of the dying cells, confirmed in the tissue sections. From our observations it is suggested that programming of cell death involves changes before endonuclease activation. Further, cell surface changes involved in the phagocytic uptake of the dying cells appear to be as precocious as endonuclease activation.

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