Several articles read new advances in the field of "Iron Death"!

!--webeditor: page title"--In this article, the small compilation of a number of important research results, together focus on scientists in the "iron death" research field of new achievements, share to everyone! Photo Credit: University of MichigRogel Cancer Center 1 Nature: Identifying Cancer Cells to Avoid Iron Death New Mechanism doi: 10.1038/s41586-019-1707-0 Chemotherapy kills them by preventing cancer cells from proliferating and inducing "cell death". A form of
cell death, called ferroptosis--- the death of iron-dependent cells--- is caused by the degradation of fat (lipid) that makes up the cell membrane.
many invasive and drug-resistant cancers are susceptible to iron death, but in a new study, researchers from research institutions such as the University of Wuerzburg and the Helmholtz Munich Center in Germany have discovered a new mechanism that makes cancer cells resistant to iron death.
this provides a new target for developing drugs that inhibit this new discovery mechanism and allow iron to die in susceptible cancer cells.
the findings are published in the journal Nature.
researchers say finding new ways in which cells gain resistance will allow us to design drugs that target this mechanism.
in fact, we already have the lead drugs that we have developed previously to indirectly target this mechanism, and we are testing them in the laboratory; iron death depends on the oxidation of lipids in cell membranes--- causing them to degrade.
it is well known that a molecule called glutathione peroxidase 4 (GPX4) reverses this process and thus acts as a lipid antioxidant, with some drugs that target GPX4, but most cancers are still resistant to iron death.
: Chinese and U.S. scientists have revealed that the intercellular interaction sourcin-mediated regulates the iron death mechanism of cancer cells doi: 10.1038/s41586-019-1426-6 iron death (ferroptosis) is a cell death process driven by cell metabolism and iron-dependent lipid peroxidation.
it is associated with ischemic organ damage and diseases such as cancer.
glutathione peroxidase 4 (GPX4) is a vital regulator of iron death, protecting cells by neutralising lipid peroxides, which are by-products of cell metabolism.
directly inhibits GPX4, or indirectly inhibits GPX4 by removing its substrate glutathione or precursor molecules used to produce glutathione, such as cysteine, can trigger iron death.
iron death helps to enhance the anti-tumor function of several tumor-suppressing proteins, such as p53, BAP1, and Jenhuso acidase.
, however, counterintuitively, mesenchymal cancer cell cells, which are prone to metastasis and often produce resistance to various treatments, are highly sensitive to iron death.
in a new study, the Chen Zhinan team at the Chinese Air Force Military Medical University and Xuejun Jiang's team at memorial Sloan Kettering Cancer Center in the United States found that the intercellular interactions mediated by calcium-sticky proteins regulate iron death independently.
related findings, published in the journal Natue, inhibit iron death by activating intracellular NF2 (also known as Merlin Hippo) and signaling pathways, mediated by E-calcium viscoproteins in epithelial cells.
inhibition of this signal axis allows the transcription co-activation factor YAP to promote iron death by raising several iron death regulators, including ACSL4 and TFRC.
this finding provides new understanding of the mechanism seisciable observations that cancer cells with interstitial or metastasized properties are highly sensitive to iron death.
3: Major discoveries! Targetiron death is expected to enhance the efficacy of immunotherapy: 10.1038/s41586-019-1170-y In a new study, researchers from the University of Michigan and Cayman Chemical studied a little-known type of cell death, ferrocidesis.
they found that iron death occurs in tumor cells and plays a role in cancer immunity.
these findings suggest that targeting this pathway has the potential to make the most popular cancer treatments --- immunotherapy --- more effective, the findings are published in the journal Nature.
researchers say iron was defined before death, but it is not known to be associated with cancer cell death or immune cells.
this will open up a huge window for scientists to explore.
the researchers found that when immunotherapy increases the activity of T cells, it increases the level of oxidizing lipids in tumor cells, leading to iron death.
based on studies of mouse and human cancer cells, increased iron death seduthes can make immunotherapy more effective at killing cancer.
iron death is a form of cell death, unlike the more well-known and well-researched apoptosis.
it depends on iron, but little is known about it.
known to be involved in brain and kidney damage.
study is the first to link it to the death of immune-mediated cancer cells.
: Cell Rep: Cancer Defense P53 will also help cancer cells avoid iron death doi: 10.1016/j.celrep.2017.12.077 How cancer cells respond to nutritional deprivation is still not particularly clear.
in some cancer cells, the lack of cysteine induces the death of iron-dependent cells, called ferroptosis, which is different from apoptosis.
recent evidence suggests that the sensitivity of iron death may be regulated by stress response transcription factors and classic tumor suppressors p53.
To further reveal the relationship between tumor inhibitor p53 and iron death sensitivity, researchers from Stanford University School of Medicine in the United States used crispR/Cas9 genome editing, small molecule probes, and high-resolution time-lapse imaging.
results were published in the international academic journal Cell Reports.
in the study, researchers found that stable expression of wild p53 delayed the death of cysteine-induced iron, and that this delay required the involvement of the p53 transcription target gene CDKN1A (coding p21), in addition to the slow consumption of glutathione in the cell and the decline in reactive oxygen cluster levels.
!--/ewebeditor:!--webeditor: !--." - Picture Source: Trend in Cell Biology 5: Chinese Scientists Reveal New Mechanism for Liver Damage in Iron Death: 10.1 Ferroptosis: A regulatory form of necrosis found in recent years is a pattern of cell death that relies on oxidation damage to iron ions, with different characteristics than apoptosis, necrosis, or autophagy.
the death process was marked by increased cytoplasm and lipid reactive oxygen, smaller mitochondria and higher mitochondrial membrane density.
this form of death is considered a breakthrough in the treatment of tumors and numerous major diseases.
iron death is iron-dependent and can be specifically reversed by iron chelating agents, but it is not clear whether iron overload can lead to iron death, and whether the mechanism between iron death and iron metabolism, the results successfully read the mystery.
To explore the role of iron ions in the occurrence of iron death, this study introduced a number of high-speed iron accumulation gene knockout mouse models, or mouse models called hemogloby disease.
hereditary hemromatosis is a common chronic iron-loaded autosomal genetic disease.
because too much iron is stored in the liver, heart and pancreas and other substantial cells, which eventually leads to degenerative lesions of tissue organs, is an important cause of slow diseasesuch as liver disease, diabetes, heart disease, etc.
the incidence of hemoglobin in white Sebicus in Europe and the United States is very high (1/200), is the number one human liver genetic disease;
: What about "iron death" therapy that kills cancer cells? Doi: 10.1038/nchembio.2239 Cells have many forms of death, including apoptosis, autophagy, and necrosis.
in recent years, "iron death" (ferroptosis) as a new way of cell necrosis gradually entered the eyes of the people.
different from the usual cell necrosis, iron death is a regulated necrosis process.
iron death is due to the failure of the membrane fat repair enzyme, glutathione peroxidase (GPX4), resulting in the accumulation of reactive oxygen free radicals (ROS) on membrane lipids, which require the participation of iron ions.
a variety of substances and external conditions can cause iron death.
small molecule erastin reduces the acquisition of cysteine by inhibiting cysteine-glutamate exchange on the membrane, blocking the synthesis of glutathione, the base of GPX4, and thus causing the accumulation of membrane lipid ROS and iron death.
in addition, another small molecule, RSL3, as an inhibitor of GPX4, can also cause iron death.
when the GPX4 gene was struck off, the mice died of kidney failure.
iron death is associated with a variety of physiological and pathological processes such as tumor suppression, neuron aleiduring, antiviral immune response and ischemic-reperfusion injury.
from the point of view of drug development, we can promote iron death to remove harmful cancer cells, infected cells, etc., or inhibit iron death to protect healthy cells.
of course, all possible therapeutic ideas need to be based on an understanding of the mechanism of iron death.
: P53-mediated "Iron Death" inhibits tumor progression doi: 10.1038/nature14344, Wei Gu, a leading Chinese scientist in cell biology, recently published their latest research progress online in the international journal Nature, they found that the classic tumor inhibitor p53 can regulate cysteine metabolism and ROS response, mediated ferroptosis process, inhibits tumor growth, and expands the new understanding of p3.
p53 is a tumor suppressor gene, which occurs in more than 50% of all malignancies.
p53-mediated cell cycle pause, cell aging and apoptosis play an important role in inhibiting tumor development, and studies have shown that p53 on cell metabolic activity regulation is also an important means to play an anti-tumor role.
: Iron death inhibitors open up new opportunities for treatment: 10.1038/ncb3064 Scientists have discovered a new form of mechanism that controls the death of immature cells in living tissue, called ferrociphone death, and also a mechanism to reverse death.
testing this mechanism can prevent organoblast tissue damage, acute renal failure and liver damage, and help develop pharmacological treatments for these diseases.
Until now, iron death was a form of cell death, identified only in tumor cells.
but research in the journal Nature Cell Biology confirms that by removing the protein Gpx4, the process of cell death that Gpx4 is responsible for regulating can also be triggered in healthy cells.
to solve this problem, the researchers tried to understand how to control the process.
using lipid histology and extensive molecular screening, the team found a small inhibitor called Liproxstatin-1 and demonstrated that it inhibited iron death.
then scientists used the inhibitor, which found could prevent cell death in living organisms.
() More exciting take stock! Stay tuned! !--/ewebeditor:page.