scholarly journals Implication of ferroptosis in aging

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Maryam Mazhar ◽  
Ahmad Ud Din ◽  
Hamid Ali ◽  
Guoqiang Yang ◽  
Wei Ren ◽  
...  
Keyword(s):  
Cell Death ◽  
Neurological Disorders ◽  
Accelerated Aging ◽  
Underlying Mechanism ◽  
Toxic Chemicals ◽  
Whole Body ◽  
Regulated Cell Death ◽  
Age Related ◽  
The Subject ◽  
Conventional Cell

AbstractLife is indeed continuously going through the irreversible and inevitable process of aging. The rate of aging process depends on various factors and varies individually. These factors include various environmental stimuli including exposure to toxic chemicals, psychological stress whereas suffering with various illnesses specially the chronic diseases serve as endogenous triggers. The basic underlying mechanism for all kinds of stresses is now known to be manifested as production of excessive ROS, exhaustion of ROS neutralizing antioxidant enzymes and proteins leading to imbalance in oxidation and antioxidant processes with subsequent oxidative stress induced inflammation affecting the cells, tissues, organs and the whole body. All these factors lead to conventional cell death either through necrosis, apoptosis, or autophagy. Currently, a newly identified mechanism of iron dependent regulated cell death called ferroptosis, is of special interest for its implication in pathogenesis of various diseases such as cardiovascular disease, neurological disorders, cancers, and various other age-related disorders (ARD). In ferroptosis, the cell death occur neither by conventional apoptosis, necrosis nor by autophagy, rather dysregulated iron in the cell mediates excessive lipid peroxidation of accumulated lethal lipids. It is not surprising to assume its role in aging as previous research have identified some solid cues on the subject. In this review, we will highlight the factual evidences to support the possible role and implication of ferroptosis in aging in order to declare the need to identify and explore the interventions to prevent excessive ferroptosis leading to accelerated aging and associated liabilities of aging.

scholarly journals Ferrous-glutathione coupling mediates ferroptosis and frailty in Caenorhabditis elegans

2019 ◽  
Author(s):  
Nicole L. Jenkins ◽  
Simon A. James ◽  
Agus Salim ◽  
Fransisca Sumardy ◽  
Terence P. Speed ◽  
...  
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Ferrous Iron ◽  
Somatic Tissue ◽  
Glutathione Depletion ◽  
Death Process ◽  
C Elegans ◽  
Regulated Cell Death ◽  
Age Related ◽  
Ageing Rate

All eukaryotes require iron. Replication, detoxification, and a cancer-protective form of regulated cell death termed ferroptosis1, all depend on iron metabolism. Ferrous iron accumulates over adult lifetime in the Caenorhabditis elegans model of ageing2. Here we show that glutathione depletion is coupled to ferrous iron elevation in these animals, and that both occur in late life to prime cells for ferroptosis. We demonstrate that blocking ferroptosis, either by inhibition of lipid peroxidation or by limiting iron retention, mitigates age-related cell death and markedly increases lifespan and healthspan in C. elegans. Temporal scaling of lifespan is not evident when ferroptosis is inhibited, consistent with this cell death process acting at specific life phases to induce organismal frailty, rather than contributing to a constant ageing rate. Because excess age-related iron elevation in somatic tissue, particularly in brain3–5, is thought to contribute to degenerative disease6, 7, our data indicate that post-developmental interventions to limit ferroptosis may promote healthy ageing.

scholarly journals Mirror Movements in Acquired Neurological Disorders: A Mini-Review

2021 ◽  
Vol 12 ◽  
Author(s):  
Ping Liu ◽  
Yuan Yuan ◽  
Ning Zhang ◽  
Xiaoyan Liu ◽  
Lihua Yu ◽  
...  
Keyword(s):  
Neurological Disorders ◽  
Neurological Diseases ◽  
Underlying Mechanism ◽  
Contralateral Limb ◽  
Extrapyramidal Disorders ◽  
Mirror Movements ◽  
Neurological Signs ◽  
Age Related ◽  
Lateral Sclerosis ◽  
Congenital Syndrome

Mirror movements (MMs) are specifically defined as involuntary movements occurring on one side of homologous muscles when performing unilateral movements with the contralateral limb. MMs have been considered a kind of soft neurological signs, and the persistence or reappearance of MMs in adults is usually pathologic. In addition to some congenital syndrome, MMs have been also described in age-related neurological diseases including pyramidal system diseases (e.g., stroke, amyotrophic lateral sclerosis) and extrapyramidal disorders (e.g., Parkinson's disease, essential tremor). With the advances in instrumentation and detection means, subtle or subclinical MMs have been deeply studied. Furthermore, the underlying mechanism is also being further elucidated. In this mini-review, we firstly discuss the MM examination means, and then review the literature regarding MMs in individuals with acquired neurological disorders, in order to further understand the pathogenesis of MMs.

Regulating inflammation associated Ferroptosis-a treatment strategy for Parkinson disease

2021 ◽  
Vol 28 ◽  
Author(s):  
Marthandam Asokan Shibu ◽  
B. Mahalakshmi ◽  
V. Bharath Kumar
Keyword(s):  
Clinical Trials ◽  
Cell Death ◽  
Treatment Strategy ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Underlying Mechanism ◽  
Acute Injury ◽  
Brain Iron ◽  
Kidney Tumors

: Ferroptosis plays a critical regulatory role for a new kind of cell death initiating and developing an array of disorders like neurological diseases, acute injury of kidney, tumors and ischemia etc. This selective deposition of iron is one of the pathogenic reasons for PD and although it’s underlying mechanism is still unknown. In this review, the role of neuroinflammation in Parkinson’s disease (PD) leading to neurodegeneration has been discussed in detail. The accumulation of brain iron has been found in many chronic neurological disorders including PD. We have also discussed the unique features of Ferroptosis as compared to other cellular death pathways and it links in aggravating the pathology of PD. Further, the concept of targeting Ferroptosis for PD pathology and inducers and inhibitors, pharmacological drugs and clinical trials for PD candidates in phase IV stage in completed status are detailed in the respective sections.

scholarly journals Beclin1-mediated ferroptosis activation is associated with isoflurane-induced toxicity in SH-SY5Y neuroblastoma cells

2019 ◽  
Author(s):  
Ruizhu Liu ◽  
Xuefeng Li ◽  
Guoqing Zhao
Keyword(s):  
Cell Death ◽  
Cell Damage ◽  
Neuroblastoma Cells ◽  
Underlying Mechanism ◽  
Dependent Manner ◽  
High Concentration ◽  
Concentration Dependent Manner ◽  
Regulated Cell Death ◽  
Deferoxamine Mesylate ◽  
High Concentrations

Abstract The widely used inhalation anesthetic, isoflurane, potentially induces neuronal injury in clinical practice. Previous studies showed multiple forms of cell death that resulted from isoflurane-induced cytotoxicity, but the precise underlying mechanism remains poorly understood. Ferroptosis has recently been identified as a non-apoptotic form of regulated cell death. Here, we found that ferroptosis inhibitors, ferrostatin-1 and deferoxamine mesylate (DFOM), showed great efficiency in maintaining cell viability in SH-SY5Y neuroblastoma cells exposed to a high concentration of isoflurane for 24 h. We also observed that cellular chelatable iron and lipid peroxidation were increased in a concentration-dependent manner in response to isoflurane. In addition, isoflurane upregulated Beclin1 phosphorylation, followed by the formation of a Beclin1-solute carrier family 7 member 11 (SLC7A11) complex, which affected the activity of cystine/glutamate antipoter and further regulated ferroptotic cell death. Accordingly, Beclin1 overexpression aggravated isoflurane-induced cell damage by upregulating ferroptosis. This phenomenon was significantly attenuated by silencing of Beclin1 in SH-SY5Y cells. These findings indicate that Beclin1 may regulate ferroptosis in a manner involving inhibition of glutamate exchange activity of system xc(−), which is implicated in isoflurane-induced toxicity. In particular, when isoflurane is administrated at high concentrations and for an extended duration, ferroptosis is more likely to play a crucial role in isoflurane-induced toxicity.

scholarly journals Changes in ferrous iron and glutathione promote ferroptosis and frailty in aging Caenorhabditis elegans

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Nicole L Jenkins ◽  
Simon A James ◽  
Agus Salim ◽  
Fransisca Sumardy ◽  
Terence P Speed ◽  
...  
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Ferrous Iron ◽  
Healthy Aging ◽  
Somatic Tissue ◽  
Glutathione Depletion ◽  
Death Process ◽  
Regulated Cell Death ◽  
Age Related ◽  
Cell Death Process

All eukaryotes require iron. Replication, detoxification, and a cancer-protective form of regulated cell death termed ferroptosis, all depend on iron metabolism. Ferrous iron accumulates over adult lifetime in Caenorhabditis elegans. Here, we show that glutathione depletion is coupled to ferrous iron elevation in these animals, and that both occur in late life to prime cells for ferroptosis. We demonstrate that blocking ferroptosis, either by inhibition of lipid peroxidation or by limiting iron retention, mitigates age-related cell death and markedly increases lifespan and healthspan. Temporal scaling of lifespan is not evident when ferroptosis is inhibited, consistent with this cell death process acting at specific life phases to induce organismal frailty, rather than contributing to a constant aging rate. Because excess age-related iron elevation in somatic tissue, particularly in brain, is thought to contribute to degenerative disease, post-developmental interventions to limit ferroptosis may promote healthy aging.

scholarly journals Ferroptosis and Its Role in Epilepsy

2021 ◽  
Vol 15 ◽  
Author(s):  
Yuxiang Cai ◽  
Zhiquan Yang
Keyword(s):  
Cell Death ◽  
Neuronal Death ◽  
Neurological Disorders ◽  
Neuronal Damage ◽  
Epileptic Seizures ◽  
Regulatory Mechanisms ◽  
Oxygen Species ◽  
Iron Ions ◽  
Intracellular Iron ◽  
Regulated Cell Death

Epilepsy is one of the most common symptoms of many neurological disorders. The typical excessive, synchronous and aberrant firing of neurons originating from different cerebral areas cause spontaneous recurrent epileptic seizures. Prolonged epilepsy can lead to neuronal damage and cell death. The mechanisms underlying epileptic pathogenesis and neuronal death remain unclear. Ferroptosis is a newly defined form of regulated cell death that is characterized by the overload of intracellular iron ions, leading to the accumulation of lethal lipid-based reactive oxygen species (ROS). To date, studies have mainly focused on its role in tumors and various neurological disorders, including epilepsy. Current research shows that inhibition of ferroptosis is likely to be an effective therapeutic approach for epilepsy. In this review, we outline the pathogenesis of ferroptosis, regulatory mechanisms of ferroptosis, related regulatory molecules, and their effects on epilepsy, providing a new direction for discovering new therapeutic targets in epilepsy.

scholarly journals Unconventional Ways to Live and Die: Cell Death and Survival in Development, Homeostasis, and Disease

2018 ◽  
Vol 34 (1) ◽  
pp. 311-332 ◽  
Author(s):  
Swapna A. Gudipaty ◽  
Christopher M. Conner ◽  
Jody Rosenblatt ◽  
Denise J. Montell
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Barrier Function ◽  
Normal Development ◽  
New Work ◽  
Biochemical Pathway ◽  
Cell Death Pathways ◽  
Regulated Cell Death ◽  
Conventional Cell ◽  
Survival Signals

Balancing cell death and survival is essential for normal development and homeostasis and for preventing diseases, especially cancer. Conventional cell death pathways include apoptosis, a form of programmed cell death controlled by a well-defined biochemical pathway, and necrosis, the lysis of acutely injured cells. New types of regulated cell death include necroptosis, pyroptosis, ferroptosis, phagoptosis, and entosis. Autophagy can promote survival or can cause death. Newly described processes of anastasis and resuscitation show that, remarkably, cells can recover from the brink of apoptosis or necroptosis. Important new work shows that epithelia achieve homeostasis by extruding excess cells, which then die by anoikis due to loss of survival signals. This mechanically regulated process both maintains barrier function as cells die and matches rates of proliferation and death. In this review, we describe these unconventional ways in which cells have evolved to die or survive, as well as the contributions that these processes make to homeostasis and cancer.

scholarly journals Autophagy Regulation and Photodynamic Therapy: Insights to Improve Outcomes of Cancer Treatment

2021 ◽  
Vol 10 ◽  
Author(s):  
Waleska K. Martins ◽  
Renata Belotto ◽  
Maryana N. Silva ◽  
Daniel Grasso ◽  
Maynne D. Suriani ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cancer Therapy ◽  
Cancer Treatment ◽  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Light Sources ◽  
Regulated Cell Death ◽  
Age Related ◽  
Cell Death Mechanisms

Cancer is considered an age-related disease that, over the next 10 years, will become the most prevalent health problem worldwide. Although cancer therapy has remarkably improved in the last few decades, novel treatment concepts are needed to defeat this disease. Photodynamic Therapy (PDT) signalize a pathway to treat and manage several types of cancer. Over the past three decades, new light sources and photosensitizers (PS) have been developed to be applied in PDT. Nevertheless, there is a lack of knowledge to explain the main biochemical routes needed to trigger regulated cell death mechanisms, affecting, considerably, the scope of the PDT. Although autophagy modulation is being raised as an interesting strategy to be used in cancer therapy, the main aspects referring to the autophagy role over cell succumbing PDT-photoinduced damage remain elusive. Several reports emphasize cytoprotective autophagy, as an ultimate attempt of cells to cope with the photo-induced stress and to survive. Moreover, other underlying molecular mechanisms that evoke PDT-resistance of tumor cells were considered. We reviewed the paradigm about the PDT-regulated cell death mechanisms that involve autophagic impairment or boosted activation. To comprise the autophagy-targeted PDT-protocols to treat cancer, it was underlined those that alleviate or intensify PDT-resistance of tumor cells. Thereby, this review provides insights into the mechanisms by which PDT can be used to modulate autophagy and emphasizes how this field represents a promising therapeutic strategy for cancer treatment.

scholarly journals The emerging role of ferroptosis in intestinal disease

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Shu Xu ◽  
Yao He ◽  
Lihui Lin ◽  
Peng Chen ◽  
Minhu Chen ◽  
...  
Keyword(s):  
Cell Death ◽  
Neurological Disorders ◽  
Kidney Injury ◽  
Intestinal Disease ◽  
Intestinal Diseases ◽  
Ischaemia Reperfusion ◽  
Regulated Cell Death ◽  
Inflammatory Bowel ◽  
Underlying Mechanisms

AbstractFerroptosis is a newly recognised type of regulated cell death (RCD) characterised by iron-dependent accumulation of lipid peroxidation. It is significantly distinct from other RCDs at the morphological, biochemical, and genetic levels. Recent reports have implicated ferroptosis in multiple diseases, including neurological disorders, kidney injury, liver diseases, and cancer. Ferroptotic cell death has also been associated with dysfunction of the intestinal epithelium, which contributes to several intestinal diseases. Research on ferroptosis may provide a new understanding of intestinal disease pathogenesis that benefits clinical treatment. In this review, we provide an overview of ferroptosis and its underlying mechanisms, then describe its emerging role in intestinal diseases, including intestinal ischaemia/reperfusion (I/R) injury, inflammatory bowel disease (IBD), and colorectal cancer (CRC).

A Modified Chair Geometry for Whole Body Counting

1976 ◽  
Vol 15 (05) ◽  
pp. 246-247
Author(s):  
S. C. Jain ◽  
G. C. Bhola ◽  
A. Nagaratnam ◽  
M. M. Gupta
Keyword(s):  
Marked Improvement ◽  
Point Of View ◽  
Whole Body ◽  
Spatial Response ◽  
Body Counting ◽  
The Subject ◽  
Whole Body Counting ◽  
The Buddha

SummaryIn the Marinelli chair, a geometry widely used in whole body counting, the lower part of the leg is seen quite inefficiently by the detector. The present paper describes an attempt to modify the standard chair geometry to minimise this limitation. The subject sits crossed-legged in the “Buddha Posture” in the standard chair. Studies with humanoid phantoms and a volunteer sitting in the Buddha posture show that this modification brings marked improvement over the Marinelli chair both from the point of view of sensitivity and uniformity of spatial response.

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