Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 735, P. 150804 - 150804
Published: Oct. 9, 2024
Language: Английский
Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 735, P. 150804 - 150804
Published: Oct. 9, 2024
Language: Английский
Trends in Pharmacological Sciences, Journal Year: 2023, Volume and Issue: 44(9), P. 573 - 585
Published: July 25, 2023
Language: Английский
Citations
68Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 92, P. 102066 - 102066
Published: Sept. 7, 2023
Language: Английский
Citations
68Cancers, Journal Year: 2024, Volume and Issue: 16(3), P. 647 - 647
Published: Feb. 2, 2024
Copper, an essential element for various biological processes, demands precise regulation to avert detrimental health effects and potential cell toxicity. This paper explores the mechanisms of copper-induced death, known as cuproptosis, its disease implications, including cancer therapy. Copper ionophores, such elesclomol disulfiram, increase intracellular copper levels. elevation triggers oxidative stress subsequent offering implications in Additionally, ionophores disrupt mitochondrial respiration protein lipoylation, further contributing toxicity death. Potential targets biomarkers are identified, can be targeted those proteins trigger cuproptosis. The role different cancers is discussed understand therapies using nanomaterials, chelators. Furthermore, explored through diseases Wilson Menkes physiological copper. Exploring cuproptosis presents opportunity improve treatments copper-related disorders cancers, with bring significant advancements modern medicine.
Language: Английский
Citations
24International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(9), P. 4753 - 4753
Published: April 26, 2024
Wilson disease is a genetic disorder of the liver characterized by excess accumulation copper, which found ubiquitously on earth and normally enters human body in small amounts via food chain. Many interesting details were published mechanistic steps, such as generation reactive oxygen species (ROS) cuproptosis causing copper dependent cell death. In patients with disease, also, increased iron deposits that may lead to iron-related ferroptosis responsible for phospholipid peroxidation within membranes subcellular organelles. All topics are covered this review article, addition diagnostic therapeutic issues disease. Excess Cu2+ primarily leads (ROS), evidenced early experimental studies exemplified detection hydroxyl radical formation using electron spin resonance (ESR) spin-trapping method. The ROS products follows principles Haber–Weiss reaction subsequent Fenton leading copper-related cuproptosis, thereby closely connected ROS. Copper due impaired biliary excretion caused inheritable malfunctioning or missing ATP7B protein. As result, disturbed cellular homeostasis prevails liver. Released from cells limited storage capacity, toxic circulation arrives at other organs, local injury. This explains why injures not only liver, but also brain, kidneys, eyes, heart, muscles, bones, explaining multifaceted clinical features Among these depression, psychosis, dysarthria, ataxia, writing problems, dysphagia, renal tubular dysfunction, Kayser–Fleischer corneal rings, cardiomyopathy, cardiac arrhythmias, rhabdomyolysis, osteoporosis, osteomalacia, arthritis, arthralgia. addition, Coombs-negative hemolytic anemia key feature undetectable serum haptoglobin. modified Leipzig Scoring System helps diagnose Patients well-treated first-line chelators like D-penicillamine facilitate removal circulating bound albumin increase urinary excretion. Early chelation therapy improves prognosis. Liver transplantation an option viewed ultima ratio end-stage untreatable complications acute failure. finally thus be life-saving approach curative treatment replacing hepatic gene mutation. conclusion, representing molecular challenge.
Language: Английский
Citations
24Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)
Published: Jan. 22, 2025
Cuproptosis differs from other forms of cell death, such as apoptosis, necroptosis, and ferroptosis, in its unique molecular mechanisms signaling pathways. In this review, we delve into the cellular metabolic pathways copper, highlighting role copper biomolecule synthesis, mitochondrial respiration, antioxidant defense. Furthermore, elucidate relationship between cuproptosis-related genes (CRGs) cancer prognosis, analyzing their expression patterns across various tumor types impact on patient outcomes. Our review also uncovers potential therapeutic applications chelators, ionophores, copper-based nanomaterials oncology. addition, discuss emerging cuproptosis remodeling microenvironment, enhancing immune infiltration, converting "cold tumors" "hot that respond better to immunotherapy. short, underscores pivotal importance biology highlights translational a novel target.
Language: Английский
Citations
6APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(9-10), P. 1330 - 1360
Published: July 16, 2024
Language: Английский
Citations
12Advanced Therapeutics, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 3, 2025
Abstract Copper plays a pivotal role in human physiology, particularly oncology, acting both as facilitator of progression and also potential avenue for advanced therapeutic approaches. Maintaining copper homeostasis is crucial. The dysregulation implicated tumor growth through its involvement critical processes angiogenesis, proliferation, metastasis. elevation level the microenvironment (TME) activates oncogenic pathways to drive neovascularization sustained malignancies. However, same reliance on offers unique weakness that can be leveraged innovative interventions. recent advances nanomedicine enable synthesis nanostructures help modulate with precision offering multifaceted approaches copper‐based cancer therapy controlled release mechanism, optimized structures induce cuproptosis, selective eradication cells minimum systemic toxicity. This review explores dual biology, emphasizing contribution tumors emerging application targeted therapy. highlights harnessing therapies their transformative from bench bed side novel, highly effective, clinical safety.
Language: Английский
Citations
1Redox Biology, Journal Year: 2024, Volume and Issue: 76, P. 103321 - 103321
Published: Aug. 19, 2024
Cell death constitutes a critical component of the pathophysiology cardiovascular diseases. A growing array non-apoptotic forms regulated cell (RCD)-such as necroptosis, ferroptosis, pyroptosis, and cuproptosis-has been identified is intimately linked to various conditions. These RCD are governed by genetically programmed mechanisms within cell, with epigenetic modifications being common crucial regulatory method. Such include DNA methylation, RNA histone acetylation, non-coding RNAs. This review recaps roles modifications, RNAs in diseases, well which regulate key proteins involved death. Furthermore, we systematically catalog existing pharmacological agents targeting novel their action article aims underscore pivotal role precisely regulating specific pathways thus offering potential new therapeutic avenues that may prove more effective safer than traditional treatments.
Language: Английский
Citations
8Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(12), P. 10271 - 10287
Published: May 7, 2024
Language: Английский
Citations
7Critical Reviews in Oncology/Hematology, Journal Year: 2024, Volume and Issue: 197, P. 104340 - 104340
Published: April 1, 2024
Pyroptosis can be triggered through both canonical and non-canonical inflammasome pathways, involving the cleavage of gasdermin (GSDM) protein family members, like GSDMD GSDME. The impact pyroptosis on tumors is nuanced, because its role in regulating cancer progression anti-tumor immunity may vary depending tumor type, stage, location, immune status. However, cannot simply categorized as promoting or inhibiting based solely whether it acute chronic nature. interplay between intricate, with some evidence suggesting that facilitate growth, while induction could stimulate anti-cancer responses. Tumor hypoxia activates inducible factor (HIF) signaling to modulate checkpoint expression. Targeting this hypoxia-pyroptosis-immune escape axis a promising therapeutic strategy. This review highlights complex crosstalk hypoxia, pyroptosis, evasion TME.
Language: Английский
Citations
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