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PHB2 ameliorates ferroptosis and aortic aneurysm/dissection through NEDD4L-dependent ubiquitination of NCOA4 - PubMed
2 months ago
- PHB2 is significantly downregulated in aortic aneurysm/dissection (AAD) and plays a protective role.
- PHB2 overexpression mitigates ferroptosis, a form of iron-dependent cell death, in vascular smooth muscle cells (VSMCs).
- PHB2 promotes NCOA4 degradation via NEDD4L-mediated ubiquitination, limiting ferritinophagy and ferroptosis.
- Loss of PHB2 exacerbates AAD progression by increasing ferroptosis and aortic wall damage.
- The PHB2-NEDD4L-NCOA4 axis is identified as a novel regulatory pathway in AAD pathogenesis.
Therapeutic translation of traditional Chinese medicine Huangqi derived exosome like nanoparticles: targeting prostate cancer through ferroptosis activation, immune reprogramming, and microbiome modul
2 months ago
- Huangqi-derived exosome-like nanoparticles (HELNs) show potential in treating prostate cancer.
- HELNs induce ferroptosis in prostate cancer cells by downregulating GPX4 protein.
- HELNs promote M1-like macrophage polarization and increase anti-tumor probiotics in the gut.
- A new nanoparticle, siGPX4@HELNs, enhances ferroptosis and improves therapeutic outcomes.
- The study uses single-cell sequencing, 16S rDNA sequencing, and bulk-RNA sequencing for analysis.
MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via mediating glycerophospholipid metabolism - PubMed
2 months ago
- MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via glycerophospholipid metabolism in diabetic nephropathy (DN).
- Single-cell RNA sequencing identifies podocytes as central to DN, with dysregulation in ferroptosis and glycerophospholipid metabolism.
- Astragaloside IV (ASIV) shows protective effects by targeting ferroptosis, reversing diabetic transcriptional changes, and preserving podocyte integrity.
- Spatial metabolomics reveals metabolic dysregulation in renal cortex and medulla, regulated by ASIV.
- Urinary metabolic intermediates of glycerophospholipid metabolism are identified as non-invasive biomarkers for DN diagnosis.
RELA as a Diagnostic Biomarker for Parkinson's Disease by Integrating Ferroptosis, Lipid Metabolism, and Neuroinflammation - PubMed
2 months ago
- RELA is proposed as a diagnostic biomarker for Parkinson's Disease.
- The study integrates ferroptosis, lipid metabolism, and neuroinflammation in understanding Parkinson's Disease.
- Authors declare no competing interests.
- References include studies on Parkinson's disease signaling pathways, epigenetic regulation, epidemiology, and proteomic analyses.
- Key findings include the role of Lewy pathology in Parkinson's disease, consisting of crowded organelles and lipid membranes.
Longitudinal clinical and preclinical studies identify hetrombopag as a potent chelator for systemic iron overload - PubMed
2 months ago
- Iron overload (IO) is a pathological condition caused by excessive iron accumulation, leading to systemic functional impairment.
- Iron chelation therapy (ICT) is the standard treatment for transfusion-related IO, but current chelators have limitations like toxicity and administration challenges.
- Hetrombopag (HPAG), an oral thrombopoietin receptor agonist, has an iron-scavenging moiety independent of its primary activity.
- Clinical and preclinical studies show HPAG is effective as both a prophylactic and therapeutic agent for systemic IO.
- HPAG acts as a ferroptosis inhibitor by reducing toxic iron accumulation and suppressing iron-induced lipid peroxidation.
- The findings suggest targeting ferroptosis is a novel therapeutic strategy for systemic IO.
Decoding GPX4 regulation in ferroptosis: mechanisms and therapeutic implications - PubMed
2 months ago
- Ferroptosis is a regulated form of cell death driven by iron-dependent lipid peroxidation.
- GPX4, a selenoenzyme, detoxifies phospholipid hydroperoxides and acts as a key regulator of ferroptosis.
- GPX4 is involved in various pathologies, including cancer, neurodegeneration, acute renal failure, and infection.
- GPX4 regulation occurs at multiple levels: transcription, mRNA stability, and post-translational modifications.
- Post-translational modifications affecting GPX4 include ubiquitination, phosphorylation, palmitoylation, methylation, hydroxylation, and lactylation.
- Therapeutic strategies targeting GPX4 include ferroptosis inducers for cancer therapy and inhibitors to prevent ferroptosis-related damage.
TIMP3 Suppresses Oxidative Stress and Ferroptosis of Lens Epithelial Cells in Cataract Through Regulating the Keap1/Nrf2 Pathway - PubMed
2 months ago
- TIMP3 suppresses oxidative stress and ferroptosis in lens epithelial cells in cataract.
- Oxidative stress-induced lens epithelial cell death is key in cataract development.
- Ferroptosis, caused by lipid peroxide accumulation and ROS overproduction, is significant in cataract.
- TIMP3 overexpression reduces lipid peroxidation and ROS accumulation in lens epithelial cells.
- TIMP3 overexpression inactivates Keap1 and enhances Nrf2, HO-1, and GPX4 expression.
- TIMP3 overexpression delays cataract formation in rat models.
- TIMP3 knockdown has opposite effects, increasing oxidative stress and ferroptosis.
- The study suggests TIMP3 as a potential antioxidative treatment for cataract.
Huaier-derived arnicolide D induces ferroptosis in gastric cancer via SRC/TNF-mediated GPX4 inactivation - PubMed
2 months ago
- Huaier-derived arnicolide D induces ferroptosis in gastric cancer via SRC/TNF-mediated GPX4 inactivation.
- Huaier n-butanol extract (HBE) shows anticancer activity but its bioactive components and mechanisms are not fully understood.
- The study aimed to identify HBE's bioactive components and their ferroptosis-related mechanisms in gastric cancer treatment.
- Methods included in vivo mouse models, UHPLC-MS/MS, network pharmacology, cellular assays, molecular docking, and gene knockdown.
- HBE inhibited tumor growth by inducing ferroptosis, evidenced by increased 4-HNE levels and disrupted iron metabolism.
- Arnicolide D was identified as a key active component in HBE with potent antitumor activity in vitro and in vivo.
- Arnicolide D targets TNF and SRC, suppressing GPX4 expression at transcriptional and post-translational levels to promote ferroptosis.
- The findings highlight Arnicolide D as a promising dual-target ferroptosis inducer for gastric cancer treatment.
Lipid Droplet-Targeted Biomimetic Liposomes Potentiate Chemo-Ferroptosis Therapy in Leukemia - PubMed
2 months ago
- Chemotherapy is the primary treatment for leukemia, but relapse often occurs due to chemoresistant leukemia cells (LCs) in the bone marrow (BM).
- Ferroptosis-based therapies offer a promising strategy to eliminate resistant LCs.
- Cytarabine chemotherapy increases lipid droplet (LD) accumulation in BM-resident LCs, leading to ferroptosis resistance.
- A biomimetic liposome (REM@HLipo) was developed, containing RSL3 (ferroptosis inducer), elacytarabine (cytarabine prodrug), and metformin (LD disruptor).
- Metformin disrupts LDs, increasing polyunsaturated fatty acids (PUFAs) for oxidation, sensitizing LCs to RSL3-induced ferroptosis.
- REM@HLipo shows potent cytotoxicity against BM-resident LCs in AML and ALL mouse models.
- The therapy significantly reduces leukemia stem cell populations in AML models.
- This study introduces a novel chemo-ferroptosis therapeutic approach for leukemia management.
Repurposing dronedarone induces ferroptosis through GPX4 inactivation and degradation in pancreatic cancer - PubMed
2 months ago
- Repurposing dronedarone induces ferroptosis in pancreatic cancer by inactivating and degrading GPX4.
- The study involves high-throughput screening and highlights the role of autophagy and ferroptosis in cancer treatment.
- Animal experiments were approved by the Animal Experimentation Ethics Committee of Lanzhou University Second Hospital.
- No competing interests were declared by the authors.
- References include studies on intratumoral microbiota, redox signaling in the pancreas, and mechanisms of ferroptosis.
Restoring cardiolipin homeostasis mitigates cerebral ischemia-reperfusion injury by suppressing ATG5-mediated neuronal autophagy-dependent ferroptosis - PubMed
2 months ago
- Cardiolipin (CL) homeostasis is crucial in mitigating cerebral ischemia-reperfusion (I/R) injury.
- CL depletion and acyl chain remodeling occur in peri-infarct brain tissues post I/R injury.
- Extracellular vesicles (EVs) contribute to CL loss; inhibiting EV release restores neuronal CL levels.
- SS-31 peptide inhibits CL release, preserves CL content, and restores CL homeostasis.
- Restoring CL homeostasis attenuates I/R injury by suppressing neuronal ferroptosis.
- SS-31 downregulates autophagy-associated genes, with ATG5 as a key target.
- Activating autophagy or overexpressing ATG5 reverses SS-31's protective effects.
- Plasma CL levels in stroke patients correlate with 90-day functional outcomes.
- SS-31 offers a novel therapeutic avenue for stroke by targeting CL homeostasis and autophagy-dependent ferroptosis.
Shenkang Injection Prevents Contrast-Induced Nephropathy by Regulating Ferroptosis Via the STAT3/HIF-1α/HMOX-1 Pathways - PubMed
2 months ago
- Shenkang Injection (SKI) prevents Contrast-Induced Nephropathy (CIN) by regulating ferroptosis via the STAT3/HIF-1α/HMOX-1 pathways.
- CIN is the third most common cause of acute renal damage in inpatient settings, with scarce effective therapies and uncertain pathophysiology.
- Network pharmacology identified 15 potential ferroptosis-related targets of SKI for preventing CIN, with the HIF-1 signaling pathway playing a critical role.
- In vivo experiments showed that contrast agents induce CIN under specific conditions, with biomarkers and electron microscopy supporting ferroptosis occurrence.
- Ferrostatin-1 (Fer-1) and SKI treatment downregulated STAT3, HIF-1α, and HMOX-1, mitigating CIN by suppressing ferroptosis.
- SKI reduces ferroptosis in HK-2 cells induced by contrast medium, suggesting its potential as an effective multi-target therapy for CIN.
Vitamin B2 metabolism promotes FSP1 stability to prevent ferroptosis - PubMed
2 months ago
- Ferroptosis is a regulated form of cell death driven by excessive lipid peroxidation and is a promising therapeutic target in cancer.
- Ferroptosis suppressor protein 1 (FSP1) is a critical regulator of ferroptosis resistance, but its expression and stability mechanisms are not well understood.
- CRISPR-Cas9 screens identified riboflavin kinase and FAD synthase, enzymes essential for synthesizing FAD from vitamin B2, as key contributors to FSP1 stability.
- FAD binding is crucial for both FSP1 activity and stability; deficiency or mutations blocking FSP1-FAD binding trigger degradation via the ubiquitin-proteasome pathway involving E3 ligase RNF8.
- Vitamin B2 supports ferroptosis resistance through FAD cofactor binding, ensuring FSP1 stability and function, unlike other vitamins that scavenge radicals.
- This study highlights a novel link between vitamin B2 metabolism and ferroptosis resistance, with potential therapeutic implications for cancer targeting FSP1.
Riboflavin metabolism shapes FSP1-driven ferroptosis resistance - PubMed
2 months ago
- Riboflavin (vitamin B2) metabolism influences FSP1-driven ferroptosis resistance.
- FSP1 (ferroptosis suppressor protein 1) is a critical inhibitor of ferroptosis, aiding in the regeneration of membrane-embedded antioxidants.
- A CRISPR-Cas9 screen identified riboflavin as a key modulator of ferroptosis sensitivity, supporting FSP1 stability and antioxidant recycling.
- The riboflavin antimetabolite roseoflavin impairs FSP1 function, sensitizing cancer cells to ferroptosis.
- Targeting riboflavin metabolism presents a therapeutic strategy to modulate the FSP1-antioxidant pathway and enhance ferroptosis sensitivity.
Targeting the OXNAD1-PTGS2 axis with resveratrol overcomes ferroptosis Inhibition and reverses 5-FU resistance in gastric cancer - PubMed
2 months ago
- 5-Fluorouracil (5-FU) is a first-line chemotherapy for gastric cancer, but resistance reduces its efficacy.
- Ferroptosis suppression is a key mechanism of chemoresistance, with mitochondrial processes not well understood.
- OXNAD1, a mitochondrial oxidoreductase, is overexpressed in gastric cancer and linked to poor prognosis and 5-FU resistance.
- OXNAD1 binds to and inhibits PTGS2, a ferroptosis driver, reducing lipid peroxidation and mitochondrial damage, thus promoting resistance.
- Resveratrol disrupts the OXNAD1-PTGS2 interaction by binding OXNAD1, restoring ferroptosis and enhancing 5-FU's cytotoxic effect in resistant cells.
- In vivo studies show resveratrol boosts 5-FU's antitumor efficacy in xenograft models.
- Targeting the OXNAD1-PTGS2 axis with resveratrol offers a promising strategy to overcome 5-FU resistance in gastric cancer.
Ferritin in ferroptosis: Implications for neurodegenerative diseases (Review) - PubMed
2 months ago
- Ferroptosis, an iron-dependent form of cell death, plays a key role in neurodegenerative diseases like Alzheimer's and Parkinson's.
- Ferritin regulates iron homeostasis by sequestering excess iron, protecting cells from Fenton reaction toxicity.
- Ferritinophagy, the degradation of ferritin, releases toxic iron, triggering ferroptosis and contributing to neurodegeneration.
- Ferritin may serve as a biomarker for early diagnosis and a target for therapeutic strategies in neurodegenerative diseases.
- MRI-based non-invasive quantification of cerebral iron deposition offers clinical translational value for monitoring disease progression.
AS1411-aptamer-functionalized DNA tetrahedron for targeted delivery of vorinostat to suppress gastric cancer progression via ferroptosis induction and epithelial-mesenchymal transition inhibition - Pu
2 months ago
- AS1411-aptamer-functionalized DNA tetrahedron (TAV) delivers vorinostat to target gastric cancer (GC).
- Vorinostat enhances p53 stability by promoting acetylation and inhibiting degradation, leading to dual antitumor effects.
- The drug promotes ferroptosis via the SLC7A11/GPX4 axis and suppresses EMT by downregulating N-cadherin, vimentin, and MMP9.
- Vorinostat also inhibits the PI3K/AKT/mTOR pathway independently of p53, enhancing anti-tumor efficacy.
- TAV demonstrates effective drug delivery, improving vorinostat's solubility and targeting efficiency in GC therapy.
- In vitro and in vivo studies confirm TAV's therapeutic effects and biocompatibility in GC models.
Indole-3-carbinol attenuates cisplatin-induced premature ovarian failure by activating Nrf2 through competitive binding of Keap1 - PubMed
2 months ago
- Indole-3-carbinol (I3C) attenuates cisplatin-induced premature ovarian failure (POF) by activating Nrf2 through competitive binding to Keap1.
- Nrf2 knockout (Nrf2-KO) mice showed decreased levels of Gpx4 and Slac7a11, increased oxidative stress, and fibrosis, similar to cisplatin-induced damage.
- I3C treatment or Nrf2 overexpression reduced cisplatin-induced ferroptosis in vitro, while Nrf2 knockdown or inhibition nullified I3C's protective effects.
- Nrf2-KO mice exhibited POF phenotypes, and I3C's protective effects were lost in these mice.
- I3C activates Nrf2 by competitively binding to Keap1 residues Y334, S363, and R380.
- Nrf2 inhibits ferroptosis by regulating NNT to maintain redox balance; NNT overexpression reversed oxidative damage from Nrf2 loss.
- The study clarifies Nrf2's role in ovarian function and identifies I3C as a potential drug to alleviate ovarian damage.
Liquiritigenin targets transferrin receptor to potentiate ferroptosis sensitivity in colorectal cancer cells - PubMed
2 months ago
- Liquiritigenin (LIQ) identified as a ferroptosis sensitizer in colorectal cancer (CRC) cells.
- LIQ stabilizes transferrin receptor (TFRC) by inhibiting its ubiquitination and degradation.
- Stabilization of TFRC leads to increased intracellular iron and lipid peroxidation, sensitizing cells to ferroptosis.
- LIQ synergizes with ferroptosis inducers (sulfasalazine or RSL3) to suppress tumor growth in vivo and ex vivo.
- Highlights LIQ's potential as a dietary intervention in CRC therapy.
BZW1 Drives Immune Evasion in Lung Adenocarcinoma via Ferroptosis Suppression - PubMed
2 months ago
- BZW1 promotes immune evasion in lung adenocarcinoma (LUAD) by suppressing ferroptosis.
- Ferroptosis is a form of programmed cell death driven by iron-dependent lipid peroxidation and is crucial for anti-tumor immunity.
- BZW1 inhibits ferroptosis by preventing FTH1 degradation via autophagic degradation of NCOA4.
- BZW1 competitively binds with NCOA4, disrupting the FTH1-NCOA4 interaction and inhibiting ferritinophagy-mediated ferritin degradation.
- Suppression of ferroptosis by BZW1 leads to an immunosuppressive microenvironment by reducing immunogenic cell death and impairing T cell activation.
- Targeting the BZW1-ferroptosis axis may enhance the efficacy of immunotherapy in LUAD.

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#ferroptosis

PHB2 ameliorates ferroptosis and aortic aneurysm/dissection through NEDD4L-dependent ubiquitination of NCOA4 - PubMed

Therapeutic translation of traditional Chinese medicine Huangqi derived exosome like nanoparticles: targeting prostate cancer through ferroptosis activation, immune reprogramming, and microbiome modul

MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via mediating glycerophospholipid metabolism - PubMed

RELA as a Diagnostic Biomarker for Parkinson's Disease by Integrating Ferroptosis, Lipid Metabolism, and Neuroinflammation - PubMed

Longitudinal clinical and preclinical studies identify hetrombopag as a potent chelator for systemic iron overload - PubMed

Decoding GPX4 regulation in ferroptosis: mechanisms and therapeutic implications - PubMed

TIMP3 Suppresses Oxidative Stress and Ferroptosis of Lens Epithelial Cells in Cataract Through Regulating the Keap1/Nrf2 Pathway - PubMed

Huaier-derived arnicolide D induces ferroptosis in gastric cancer via SRC/TNF-mediated GPX4 inactivation - PubMed

Lipid Droplet-Targeted Biomimetic Liposomes Potentiate Chemo-Ferroptosis Therapy in Leukemia - PubMed

Repurposing dronedarone induces ferroptosis through GPX4 inactivation and degradation in pancreatic cancer - PubMed

Restoring cardiolipin homeostasis mitigates cerebral ischemia-reperfusion injury by suppressing ATG5-mediated neuronal autophagy-dependent ferroptosis - PubMed

Shenkang Injection Prevents Contrast-Induced Nephropathy by Regulating Ferroptosis Via the STAT3/HIF-1α/HMOX-1 Pathways - PubMed

Vitamin B2 metabolism promotes FSP1 stability to prevent ferroptosis - PubMed

Riboflavin metabolism shapes FSP1-driven ferroptosis resistance - PubMed

Targeting the OXNAD1-PTGS2 axis with resveratrol overcomes ferroptosis Inhibition and reverses 5-FU resistance in gastric cancer - PubMed

Ferritin in ferroptosis: Implications for neurodegenerative diseases (Review) - PubMed

AS1411-aptamer-functionalized DNA tetrahedron for targeted delivery of vorinostat to suppress gastric cancer progression via ferroptosis induction and epithelial-mesenchymal transition inhibition - Pu

Indole-3-carbinol attenuates cisplatin-induced premature ovarian failure by activating Nrf2 through competitive binding of Keap1 - PubMed

Liquiritigenin targets transferrin receptor to potentiate ferroptosis sensitivity in colorectal cancer cells - PubMed

BZW1 Drives Immune Evasion in Lung Adenocarcinoma via Ferroptosis Suppression - PubMed