We are analyzing https://link.springer.com/article/10.1007/s00204-023-03625-x.

Title:
Ferroptosis: potential targets and emerging roles in pancreatic diseases | Archives of Toxicology
Description:
Ferroptosis is a newly discovered form of regulatory cell death characterized by excessive iron-dependent lipid peroxidation. In the past decade, significant breakthroughs have been made in comprehending the features and regulatory mechanisms of ferroptosis, and it has been confirmed that ferroptosis plays a pivotal role in the pathophysiological processes of various diseases, including tumors, inflammation, neurodegenerative diseases, and infectious diseases. The pancreas, which is the second largest digestive gland in the human body and has both endocrine and exocrine functions, is a vital organ for controlling digestion and metabolism. In recent years, numerous studies have confirmed that ferroptosis is closely related to pancreatic diseases, which is attributed to abnormal iron accumulation, as an essential biochemical feature of ferroptosis, is often present in the pathological processes of various pancreatic exocrine and endocrine diseases and the vulnerability of the pancreas to oxidative stress stimulation and damage. Therefore, comprehending the regulatory mechanism of ferroptosis in pancreatic diseases may provide valuable new insights into treatment strategies. In this review, we first summarize the hallmark features of ferroptosis and then analyze the exact mechanisms by which ferroptosis is precisely regulated at multiple levels and links, including iron metabolism, lipid metabolism, the GPX4-mediated ferroptosis defense system, the GPX4-independent ferroptosis defense system, and the regulation of autophagy on ferroptosis. Finally, we discuss the role of ferroptosis in the occurrence and development of pancreatic diseases and summarize the feasibility and limitations of ferroptosis as a therapeutic target for pancreatic diseases.
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Keywords {🔍}

pubmed, article, google, scholar, cas, ferroptosis, central, cell, cancer, httpsdoiorgs, biol, death, nat, pancreatic, diabetes, liu, wang, lipid, iron, cells, diabetic, res, zhang, role, metabolism, autophagy, sun, pancreatitis, gpx, kang, chem, stress, pathway, sci, chen, diseases, peroxidation, oxidative, mol, nature, yang, tang, mechanisms, ferroptotic, promotes, commun, rev, acute, httpsdoiorg, inhibition,

Topics {✒️}

pancreatic ductal adenocarcinoma ripk1/nf-κb/aqp8 pathway long-chain acyl-coa synthetase-4 mir-200b-3p/cofilin-2 axis cd36/pink/parkin pathway leading month download article/chapter perk-nrf2-ho-1 signaling pathway diet-induced phospholipid remodeling p62-keap1-nrf2 pathway protects diabetes-induced cardiac malfunction p53-mediated ferroptotic responses early intra-acinar events hif-1α/ho-1 pathway p62-keap1-nrf2 pathway blood-brain barrier destruction yap/taz drives alterations ros/ho-1/gpx4 axis autophagy-dependent cell death glutathione-independent ferroptosis suppressor copper-dependent autophagic degradation genotype-selective antitumor agents aif-mediated cell death gpx4 inhibitor-induced ferroptosis activating autophagy-dependent ferroptosis ferroptosis-inducing agents compromise oxidative stress-induced apoptosis p53-mediated tumour suppression article huang related subjects full article pdf dhodh-mediated ferroptosis defence db/db mouse model ferritinophagy-mediated ferritin turnover regulated cell death aggravate acute pancreatitis nrf2-keap1 signaling transcription factor yy1 ampk/nrf2 pathways ferroptotic cell death cisd2 promotes ferroptosis p53-mediated activity kagan ve controls intracellular trafficking mancias jd autophagy promotes ferroptosis p53-mediated ferroptosis autophagy-dependent modulation autophagy-dependent ferroptosis autophagy dependent degradation privacy choices/manage cookies

Questions {❓}

Evans JL, Goldfine ID, Maddux BA, Grodsky GM (2003) Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction?
Feng H, Stockwell BR (2018) Unsolved mysteries: how does lipid peroxidation cause ferroptosis?
Li L, Yu XJ, Gao L, Cheng L, Sun B, Wang G (2022b) Diabetic ferroptosis and pancreatic cancer: foe or friend?
Moore AR, Rosenberg SC, McCormick F, Malek S (2020) RAS-targeted therapies: is the undruggable drugged?
Stoyanovsky DA, Tyurina YY, Shrivastava I et al (2019) Iron catalysis of lipid peroxidation in ferroptosis: regulated enzymatic or random free radical reaction?

Schema {🗺️}

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         description:Ferroptosis is a newly discovered form of regulatory cell death characterized by excessive iron-dependent lipid peroxidation. In the past decade, significant breakthroughs have been made in comprehending the features and regulatory mechanisms of ferroptosis, and it has been confirmed that ferroptosis plays a pivotal role in the pathophysiological processes of various diseases, including tumors, inflammation, neurodegenerative diseases, and infectious diseases. The pancreas, which is the second largest digestive gland in the human body and has both endocrine and exocrine functions, is a vital organ for controlling digestion and metabolism. In recent years, numerous studies have confirmed that ferroptosis is closely related to pancreatic diseases, which is attributed to abnormal iron accumulation, as an essential biochemical feature of ferroptosis, is often present in the pathological processes of various pancreatic exocrine and endocrine diseases and the vulnerability of the pancreas to oxidative stress stimulation and damage. Therefore, comprehending the regulatory mechanism of ferroptosis in pancreatic diseases may provide valuable new insights into treatment strategies. In this review, we first summarize the hallmark features of ferroptosis and then analyze the exact mechanisms by which ferroptosis is precisely regulated at multiple levels and links, including iron metabolism, lipid metabolism, the GPX4-mediated ferroptosis defense system, the GPX4-independent ferroptosis defense system, and the regulation of autophagy on ferroptosis. Finally, we discuss the role of ferroptosis in the occurrence and development of pancreatic diseases and summarize the feasibility and limitations of ferroptosis as a therapeutic target for pancreatic diseases.
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            Biomedicine
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      description:Ferroptosis is a newly discovered form of regulatory cell death characterized by excessive iron-dependent lipid peroxidation. In the past decade, significant breakthroughs have been made in comprehending the features and regulatory mechanisms of ferroptosis, and it has been confirmed that ferroptosis plays a pivotal role in the pathophysiological processes of various diseases, including tumors, inflammation, neurodegenerative diseases, and infectious diseases. The pancreas, which is the second largest digestive gland in the human body and has both endocrine and exocrine functions, is a vital organ for controlling digestion and metabolism. In recent years, numerous studies have confirmed that ferroptosis is closely related to pancreatic diseases, which is attributed to abnormal iron accumulation, as an essential biochemical feature of ferroptosis, is often present in the pathological processes of various pancreatic exocrine and endocrine diseases and the vulnerability of the pancreas to oxidative stress stimulation and damage. Therefore, comprehending the regulatory mechanism of ferroptosis in pancreatic diseases may provide valuable new insights into treatment strategies. In this review, we first summarize the hallmark features of ferroptosis and then analyze the exact mechanisms by which ferroptosis is precisely regulated at multiple levels and links, including iron metabolism, lipid metabolism, the GPX4-mediated ferroptosis defense system, the GPX4-independent ferroptosis defense system, and the regulation of autophagy on ferroptosis. Finally, we discuss the role of ferroptosis in the occurrence and development of pancreatic diseases and summarize the feasibility and limitations of ferroptosis as a therapeutic target for pancreatic diseases.
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