Ferroptosis in Myocardial Infarction:An Epiphenomenon or Not (Preprint)

2020 ◽  
Author(s):  
Sheng Kang
Keyword(s):  
Neurological Diseases ◽  
Therapeutic Targets ◽  
Iron Chelator ◽  
Organ Damage ◽  
Vital Role ◽  
Pathological Process ◽  
Cardiac Biomarkers ◽  
Death Process ◽  
Voltage Dependent ◽  
Cell Death Process

UNSTRUCTURED Identification of effective cardiac biomarkers and therapeutic targets for myocardial infarction (MI) will play an important role in early diagnosis and the improving prognosis. Ferroptosis, a cell death process driven by cellular metabolism and iron-dependent lipid peroxidation, has been implicated in diseases such as ischaemic organ damage, cancer, and neurological diseases. Its modulators were involved in transferrin receptor, iron chelator, and clock protein ARNTL, etc. Its mechanisms included the inhibition of the system XC-, the diminished GPX4 activity, the change of mitochondrial voltage-dependent anion channels, and the rising intracellular ROS level, etc. Further, the inhibitors of apoptosis, pyroptosis and autophagy did not prevent the occurrence of ferroptosis, but iron chelating agents and antioxidants could inhibit it. Noticeably, ferroptosis is an important pattern of cardiomyocyte death in the infarcted area, which may play a vital role in support of myocardial pathological process of heart disease. However, the molecular mechanism of ferroptosis in the pathogenesis and development of MI is not clear. Therefore, a greater depth of exploration of the mechanism of ferroptosis in MI and ferroptosis inhibitors will undoubtedly improve the pathological process of MI, which is expected to identify ferroptosis as novel diagnostic and therapeutic targets of MI.

scholarly journals Ferroptosis in myocardial infarction: not a marker but a maker

Open Biology ◽  
2021 ◽  
Vol 11 (4) ◽  
Author(s):  
Xiao-dong Wang ◽  
Sheng Kang
Keyword(s):  
Myocardial Infarction ◽  
Neurological Diseases ◽  
Therapeutic Targets ◽  
Iron Chelator ◽  
Organ Damage ◽  
Vital Role ◽  
Pathological Process ◽  
Cardiac Biomarkers ◽  
Death Process ◽  
Voltage Dependent

Identification of effective cardiac biomarkers and therapeutic targets for myocardial infarction (MI) will play an important role in early diagnosis and improving prognosis. Ferroptosis, a cell death process driven by cellular metabolism and iron-dependent lipid peroxidation, has been implicated in diseases such as ischaemic organ damage, cancer and neurological diseases. Its modulators were involved in transferrin receptor, iron chelator, clock protein ARNTL, etc. Its mechanisms included the inhibition of system X C − , diminished GPX4 activity, change of mitochondrial voltage-dependent anion channels and rising intracellular reactive oxygen species level. Further, the inhibitors of apoptosis, pyroptosis and autophagy did not prevent the occurrence of ferroptosis, but iron chelating agents and antioxidants could inhibit it. Noticeably, ferroptosis is an important pattern of cardiomyocyte death in the infarcted area, which may play a vital role in support of the myocardial pathological process of heart disease. However, the molecular mechanism of ferroptosis in the pathogenesis and the development of MI is not clear. Therefore, a greater depth of exploration of the mechanism of ferroptosis and its inhibitors will undoubtedly improve the pathological process of MI, which may be expected to identify ferroptosis as novel diagnostic and therapeutic targets of MI.

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 Stability of selected reference genes in Sf9 cells treated with extrinsic apoptotic agents

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Benshui Shu ◽  
Jingjing Zhang ◽  
Jie Zeng ◽  
Gaofeng Cui ◽  
Guohua Zhong
Keyword(s):  
Reference Genes ◽  
Target Genes ◽  
High Sensitivity ◽  
Vital Role ◽  
Death Process ◽  
Sf9 Cells ◽  
Accurate Normalization ◽  
Stability Ranking ◽  
Cell Death Process ◽  
Accuracy Of Results

Abstract As a tightly controlled cell death process, apoptosis eliminates unwanted cells and plays a vital role in multicellular organisms. Previous study have demonstrated that apoptosis occurred in Spodoptera frugiperda cultured Sf9 cells, which triggered by diverse apoptotic stimuli, including azadirachtin, camptothecin and ultraviolet. Due to its simplicity, high sensitivity and reliable specificity, RT-qPCR has been used widespread for analyzing expression levels of target genes. However, the selection of reference genes influences the accuracy of results profoundly. In this study, eight genes were selected for analyses of their suitability as references for normalizing RT-PCR data in Sf9 cells treated with apoptotic agents. Five algorithms, including NormFinder, BestKeeper, Delta Ct method, geNorm, and RefFinder, were used for stability ranking. Based on comprehensively analysis, the expression stability of selected genes varied in cells with different apoptotic stimuli. The best choices for cells under different apoptosis conditions were listed: EF2 and EF1α for cells treated with azadirachtin; RPL13 and RPL3 for cells treated with camptothecin; EF1α and β-1-TUB for cells irradiated under ultraviolet; and EF1α and EF2 for combinational analyses of samples. Our results not only facilitate a more accurate normalization for RT-qPCR data, but also provide the reliable assurance for further studies of apoptotic mechanisms under different stimulus in Sf9 cells.

scholarly journals Advances in the Relationship Between Pyroptosis and Diabetic Neuropathy

2021 ◽  
Vol 9 ◽  
Author(s):  
Jingyu Xu ◽  
Shufang Cai ◽  
Jiaxin Zhao ◽  
Ke Xu ◽  
Hao Ji ◽  
...  
Keyword(s):  
Neurological Diseases ◽  
Cerebrovascular Diseases ◽  
Cell Swelling ◽  
Death Process ◽  
Interleukin 18 ◽  
The People ◽  
Cell Death Process ◽  
The Relationship ◽  
Regulatory Significance

Pyroptosis is a novel programmed cell death process that promotes the release of interleukin-1β (IL-1β) and interleukin-18 (IL-18) by activating inflammasomes and gasdermin D (GSDMD), leading to cell swelling and rupture. Pyroptosis is involved in the regulation of the occurrence and development of cardiovascular and cerebrovascular diseases, tumors, and nerve injury. Diabetes is a metabolic disorder characterized by long-term hyperglycemia, insulin resistance, and chronic inflammation. The people have paid more and more attention to the relationship between pyroptosis, diabetes, and its complications, especially its important regulatory significance in diabetic neurological diseases, such as diabetic encephalopathy (DE) and diabetic peripheral neuropathy (DPN). This article will give an in-depth overview of the relationship between pyroptosis, diabetes, and its related neuropathy, and discuss the regulatory pathway and significance of pyroptosis in diabetes-associated neuropathy.

scholarly journals Mechanisms of Intranasal Deferoxamine in Neurodegenerative and Neurovascular Disease

2021 ◽  
Vol 14 (2) ◽  
pp. 95
Author(s):  
Jacob Kosyakovsky ◽  
Jared Fine ◽  
William Frey ◽  
Leah Hanson
Keyword(s):  
Targeted Delivery ◽  
Cognitive Aging ◽  
Brain Aging ◽  
Neurological Diseases ◽  
Iron Chelation ◽  
Iron Chelator ◽  
Modern Medicine ◽  
Potential Applicability ◽  
Disease Modifying ◽  
Further Development

Identifying disease-modifying therapies for neurological diseases remains one of the greatest gaps in modern medicine. Herein, we present the rationale for intranasal (IN) delivery of deferoxamine (DFO), a high-affinity iron chelator, as a treatment for neurodegenerative and neurovascular disease with a focus on its novel mechanisms. Brain iron dyshomeostasis with iron accumulation is a known feature of brain aging and is implicated in the pathogenesis of a number of neurological diseases. A substantial body of preclinical evidence and early clinical data has demonstrated that IN DFO and other iron chelators have strong disease-modifying impacts in Alzheimer’s disease (AD), Parkinson’s disease (PD), ischemic stroke, and intracranial hemorrhage (ICH). Acting by the disease-nonspecific pathway of iron chelation, DFO targets each of these complex diseases via multifactorial mechanisms. Accumulating lines of evidence suggest further mechanisms by which IN DFO may also be beneficial in cognitive aging, multiple sclerosis, traumatic brain injury, other neurodegenerative diseases, and vascular dementia. Considering its known safety profile, targeted delivery method, robust preclinical efficacy, multiple mechanisms, and potential applicability across many neurological diseases, the case for further development of IN DFO is considerable.

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 TSPO: kaleidoscopic 18-kDa amid biochemical pharmacology, control and targeting of mitochondria

2016 ◽  
Vol 473 (2) ◽  
pp. 107-121 ◽  
Author(s):  
Jemma Gatliff ◽  
Michelangelo Campanella
Keyword(s):  
Neurological Diseases ◽  
Anion Channel ◽  
Translocator Protein ◽  
Endocrine Regulation ◽  
Voltage Dependent Anion Channel ◽  
Steroid Synthesis ◽  
Cellular Processes ◽  
Cellular Events ◽  
Voltage Dependent

The 18-kDa translocator protein (TSPO) localizes in the outer mitochondrial membrane (OMM) of cells and is readily up-regulated under various pathological conditions such as cancer, inflammation, mechanical lesions and neurological diseases. Able to bind with high affinity synthetic and endogenous ligands, its core biochemical function resides in the translocation of cholesterol into the mitochondria influencing the subsequent steps of (neuro-)steroid synthesis and systemic endocrine regulation. Over the years, however, TSPO has also been linked to core cellular processes such as apoptosis and autophagy. It interacts and forms complexes with other mitochondrial proteins such as the voltage-dependent anion channel (VDAC) via which signalling and regulatory transduction of these core cellular events may be influenced. Despite nearly 40 years of study, the precise functional role of TSPO beyond cholesterol trafficking remains elusive even though the recent breakthroughs on its high-resolution crystal structure and contribution to quality-control signalling of mitochondria. All this along with a captivating pharmacological profile provides novel opportunities to investigate and understand the significance of this highly conserved protein as well as contribute the development of specific therapeutics as presented and discussed in the present review.

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
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