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Persistent PI3K-AKT signaling fortifies cellular defense against oxidative stress and ferroptosis through augmented mitochondrial fitness - PubMed
2 months ago
- Persistent PI3K-AKT signaling enhances cellular defense against oxidative stress and ferroptosis.
- The study highlights the role of augmented mitochondrial fitness in this protective mechanism.
- Key topics include Ferroptosis resistance, Mitochondrial fitness, Oncogenic pathways, Oxidative stress, and PI3K–AKT signaling.
- The authors declare no competing interests and all approved the final version for publication.
- References include studies on reactive oxygen species (ROS), redox regulation, and their roles in cancer and cellular responses.
LINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma - PubMed
2 months ago
- Ferroptosis is an iron-dependent programmed cell death that inhibits tumor progression.
- MICAL2 influences p53 nuclear translocation and facilitates its ubiquitination by recruiting MDM2, leading to p53 degradation.
- This process inhibits ferroptosis in nasopharyngeal carcinoma (NPC) cells, promoting NPC progression and worsening patient prognosis.
- LINC-AC092535.5, a novel lncRNA, regulates MICAL2 mRNA levels at transcriptional and post-transcriptional levels.
- Transcriptome sequencing and RACE experiments helped identify the function of LINC-AC092535.5.
- These findings expand the ferroptosis gene regulatory network and may inform new NPC treatment strategies.
Investigating the Mechanism of Rehmannia glutinosa-Ephedra sinica in heart failure with preserved ejection fraction by Network Pharmacology, Metabolomics and Experimental Validation - PubMed
2 months ago
- Study investigates Rehmannia glutinosa-Ephedra sinica (MD) for treating heart failure with preserved ejection fraction (HFpEF).
- MD improves metabolic disorders, cardiac remodeling, and diastolic dysfunction in HFpEF models.
- Mechanisms involve PI3K/AKT signaling and ferroptosis regulation via GPX4/ACSL4 pathways.
- In vitro studies show MD-containing serum attenuates palmitic acid-induced metabolic dysfunction and ferroptosis.
- Findings suggest MD's cardioprotective effects are linked to metabolic and ferroptosis modulation.
Systemic Integrative Mechanisms and Intervention Strategies in Exercise-Induced Skeletal Muscle Damage: Evidence from Animal, Clinical, and Multi-Omics Studies - PubMed
2 months ago
- Exercise-induced muscle damage (EIMD) is not just mechanical but a systems-level failure of stress integration.
- Key factors include disturbances in Ca2+ homeostasis, metabolic stress, redox imbalance, and immune activation.
- Maladaptive remodeling can lead to mitochondrial dysfunction, ferroptosis, chronic inflammation, and impaired regeneration.
- Reactive oxygen species, iron-dependent lipid peroxidation, and immune polarization are critical molecular tipping points.
- Satellite cells integrate metabolic history and epigenetic memory, linking repetitive injury to sarcopenia and metabolic disease risk.
- Multi-omics, digital monitoring, and individualized rehabilitation may enable precision management of EIMD.
The interplay between mitophagy and ferroptosis in Alzheimer's disease: Mechanisms and therapeutic implications - PubMed
2 months ago
- Alzheimer's disease (AD) is characterized by amyloid-β plaques and neurofibrillary tangles.
- Mitophagy (clearance of damaged mitochondria) and ferroptosis (iron-dependent cell death) are key processes in AD neurodegeneration.
- Impaired mitophagy disrupts redox and iron homeostasis, increasing susceptibility to ferroptosis.
- Ferroptosis events, like lipid peroxidation, worsen mitochondrial dysfunction, creating a self-amplifying cycle.
- Potential therapeutic strategies include Urolithin A and ferroptosis inhibitors.
- Targeting the mitophagy-ferroptosis loop may offer a new therapeutic approach for AD.
Human umbilical cord-derived mesenchymal stem cell exosomes ameliorate hepatocyte ferroptosis and sepsis-associated liver injury by restoring iron homeostasis in hepatocytes - PubMed
2 months ago
- Human umbilical cord-derived mesenchymal stem cell exosomes (HUMSCs-Exo) can mitigate hepatocyte ferroptosis and sepsis-associated liver injury (SALI).
- HUMSCs-Exo restore iron homeostasis in hepatocytes by modulating key proteins like FPN, xCT, GPX4, FTH1, ACSL4, and TFRC.
- These exosomes reduce intracellular lipid peroxidation and labile iron accumulation, thereby protecting against liver injury.
- The study validates findings in both murine and human hepatocyte cell lines, suggesting a novel therapeutic strategy for SALI.
AURKA-mediated destabilization of SAPS3 drives ferroptosis evasion via 7-dehydrocholesterol biosynthesis in colorectal cancer - PubMed
2 months ago
- AURKA destabilizes SAPS3, leading to ferroptosis evasion in colorectal cancer (CRC).
- AURKA-mediated phosphorylation of SAPS3 activates AMPK, inhibiting SREBP2 and DHCR7, resulting in 7-dehydrocholesterol (7-DHC) accumulation.
- 7-DHC acts as a lipid antioxidant, conferring resistance to ferroptosis.
- Inhibition of AURKA restores ferroptosis sensitivity and enhances chemotherapy efficacy in CRC models.
- High AURKA expression correlates with poor prognosis and reduced chemotherapy response in CRC patients.
- The study identifies the AURKA-SAPS3-AMPK-SREBP2 axis as a key regulator linking cholesterol metabolism to ferroptosis evasion.
LCN2 aggravates sepsis-induced ALI by inhibiting MUC1 to activate ER-stress-autophagy induced ferroptosis via lactate/MCT1/AMPK/mTOR axis - PubMed
2 months ago
- LCN2 plays a key role in aggravating sepsis-induced acute lung injury (ALI).
- The mechanism involves inhibition of MUC1, leading to activation of ER-stress-autophagy induced ferroptosis via the lactate/MCT1/AMPK/mTOR axis.
- Sorafenib was identified as a potential therapeutic compound for ALI, improving survival rates and alleviating lung injury in septic mice.
- The study utilized various methods including Western blot, Immunohistochemistry, HE staining, TEM, and lipid peroxidation activity detection.
- Findings suggest new therapeutic targets and strategies for sepsis-induced ALI.
Traditional Chinese Medicine and Ferroptosis in Alzheimer's Disease: A Potential Therapeutic Approach - PubMed
2 months ago
- Alzheimer's disease (AD) is a major neurodegenerative disorder with no current cure.
- Ferroptosis, a cell death process linked to iron dysregulation and lipid peroxidation, plays a key role in AD.
- Traditional Chinese Medicine (TCM) shows potential in managing AD by targeting ferroptosis pathways.
- TCM interventions include herbal extracts, monomers, compound formulas, and acupuncture.
- Key targets include iron homeostasis, the system Xc-/GSH/GPX4 antioxidant system, and the Keap1/Nrf2/ARE pathway.
- Current evidence is mostly preclinical, with challenges like blood-brain barrier penetration and standardization.
- TCM offers promising avenues for AD treatment by modulating ferroptosis.
Insights into the potential pathogenesis and therapeutic implications of ferroptosis in brain microvascular endothelial cells during stroke - PubMed
2 months ago
- Ferroptosis, an iron-dependent cell death pathway, plays a key role in stroke-related brain injury.
- Brain microvascular endothelial cells (BMECs) are crucial for Blood-Brain Barrier (BBB) integrity.
- BMEC ferroptosis contributes to stroke pathogenesis by compromising BBB, causing edema, and increasing neuroinflammation.
- Key signaling pathways like Meg3/p53/GPX4 and TEAD1/MMP3 regulate BMEC ferroptosis.
- Therapeutic strategies include iron chelators, genetic interventions, nanodelivery systems, and selenium compounds.
- The study aims to provide insights for neuroprotective therapies targeting BMEC ferroptosis in stroke.
The hippo-YAP1/TEAD1-SLC7A5 axis: uncovering a novel therapeutic target for oxalate-induced renal tubular ferroptosis - PubMed
2 months ago
- The study investigates the regulatory mechanisms of ferroptosis in renal tubular epithelial cells under high oxalate stress.
- High oxalate induces ferroptosis and activates the Hippo pathway, leading to YAP1 phosphorylation and inactivation.
- Multi-omics approaches identified YAP1 as a key regulator and SLC7A5 as its direct transcriptional target via TEAD1.
- High oxalate disrupts YAP1/TEAD1 binding to the SLC7A5 promoter, downregulating SLC7A5, which mediates ferroptosis under YAP1 inhibition.
- SLC7A5 downregulation restricts leucine availability and suppresses mTOR signaling, while leucine supplementation or mTOR reactivation reverses ferroptosis.
- The Hippo-YAP1/TEAD1-SLC7A5 axis is established as a master regulatory pathway for oxalate-induced ferroptosis, offering a therapeutic target for oxalate nephropathy.
Puerarin promotes nerve regeneration and functional recovery after peripheral nerve injury by inhibiting ACSL4-dependent ferroptosis - PubMed
2 months ago
- Puerarin (Pu) promotes nerve regeneration and functional recovery after peripheral nerve injury (PNI).
- Pu's mechanism involves inhibiting ACSL4-dependent ferroptosis, a process linked to PNI.
- RNA sequencing revealed Pu attenuates oxygen-glucose deprivation (OGD)-induced injury via ACSL4-dependent ferroptosis.
- Molecular docking showed Pu competitively binds to the ACSL4 active site, with Leu468 and Thr469 as key binding sites.
- In vivo and in vitro assays confirmed Pu improves nerve morphology, function, and electrophysiology by inhibiting ferroptosis.
- Loss-of-function studies validated ACSL4's essential role in Pu's neuroprotective effects.
- Pu is identified as a promising therapeutic strategy for ferroptosis-related diseases.
GHRHR Deficiency Enhances Retinal Ganglion Cell Survival and Visual Functions in Experimental Glaucoma by Inhibiting Ferroptosis - PubMed
2 months ago
- GHRHR deficiency enhances retinal ganglion cell (RGC) survival and visual functions in experimental glaucoma by inhibiting ferroptosis.
- GHRHR deficiency prevents downregulation of anti-ferroptotic mediators GPX4 and FTH1 and suppresses pro-ferroptotic factor ACSL4.
- GHRHR inhibition reduces iron accumulation, lipid peroxidation, and reactive oxygen species (ROS) accumulation in RGCs.
- Single-cell transcriptomic analysis reveals RGC-specific alterations in genes related to ferroptosis, lipid metabolism, oxidative stress, and mitochondrial dynamics.
- Pharmacological GHRHR inhibition in mitochondria-damaged primary RGCs reduces lipid peroxidation and mitochondrial ROS, improving RGC survival.
- GHRHR inhibition is identified as a potential therapeutic strategy for glaucomatous neurodegeneration, preserving both structural and functional retinal integrity.
Chemo-photothermal synergy ignites antitumor immunity via ferroptosis - PubMed
2 months ago
- Development of amphiphilic ferrocene-based polymer (PPEGMA-b-PFMMA) to co-encapsulate Docetaxel (Doc) and photosensitizer IR808, forming photothermally responsive nanoparticles (P8D NPs).
- P8D NPs improve aqueous stability and tumor-specific accumulation via hydrogen peroxide (H₂O₂)-triggered drug release in the tumor microenvironment.
- Near-infrared (NIR) irradiation causes P8D NPs to generate heat and reactive oxygen species (ROS), promoting drug release and nanoparticle disintegration.
- Doc induces HMGB1 translocation from nucleus to cytoplasm, while PTT/PDT facilitates extracellular release of DAMPs and tumor-associated antigens via ferroptosis and cell membrane rupture.
- Enhanced dendritic cell (DC) maturation, antigen presentation, and cytotoxic CD8+ T cell infiltration reverse the immunosuppressive tumor microenvironment.
- Combination strategy inhibits distant tumor growth and establishes long-term anti-tumor immunological memory to prevent recurrence.
- Ferrocene-based nanocarrier-mediated PTT/PDT synergizes with Doc to reactivate antitumor immunity through ferroptosis-induced immunogenic cell death (ICD).
Fisetin alleviates lipopolysaccharide-induced mastitis by inhibiting ferroptosis and modulating the gut microbiota - PubMed
2 months ago
- Fisetin (FIS) shows potential in treating bovine mastitis by reducing inflammation and oxidative stress.
- FIS inhibits ferroptosis pathways, lowering inflammatory cytokines in mammary tissues.
- Treatment with FIS alters gut microbiota and increases short-chain fatty acids (SCFAs), aiding mastitis recovery.
- The study suggests FIS as a novel, antibiotic-free therapeutic strategy for mastitis.
USP20 governs tyrosine kinase inhibitors resistance through ferroptosis evasion by targeting GPX4 in cancers - PubMed
2 months ago
- USP20 is identified as a key driver of resistance to tyrosine kinase inhibitors (TKIs) like sunitinib and sorafenib in cancers such as renal cell carcinoma (RCC) and lung cancer (LC).
- USP20 deubiquitinates and stabilizes GPX4, a ferroptosis suppressor, enabling cancer cells to evade ferroptosis and resist TKI treatment.
- Clinical data show co-overexpression of USP20 and GPX4 in RCC and LC patients, correlating with poor prognosis.
- Genetic ablation or pharmacological inhibition of USP20 sensitizes resistant tumors to TKIs by promoting ferroptosis, offering a new therapeutic strategy.
- The study highlights the USP20-GPX4 axis as a targetable mechanism to overcome TKI resistance in cancer therapy.
The multifaceted roles of the ACSL family in cancer: Metabolic reprogramming, ferroptosis regulation and tumour immune microenvironment remodelling - PubMed
2 months ago
- The ACSL family plays multifaceted roles in cancer, including metabolic reprogramming, ferroptosis regulation, and tumor immune microenvironment remodeling.
- ACSL isoforms (ACSL1-ACSL6) have distinct and context-dependent effects in cancer, influencing tumorigenesis, progression, and therapy response.
- ACSL1 promotes an immunosuppressive tumor immune microenvironment (TIME) via M2 macrophage polarization.
- ACSL3 and ACSL4 have antagonistic roles in ferroptosis regulation.
- ACSL5 exhibits dual effects through lipid metabolism, apoptosis, and immunity.
- ACSL6 is involved in autophagy and hematological malignancies.
- Dysregulation of ACSL isoforms correlates with tumor progression, drug resistance, and immunotherapy response.
- Emerging ACSL-targeted therapies show significant translational potential in cancer treatment.
- Future research should focus on optimizing isoform-selective inhibitors and exploring synergistic effects with existing therapies like immune checkpoint inhibitors and radiotherapy.
Doxorubicin induces ferroptosis in endometrial cancer by suppressing the MKK6/p38/CEBPB axis - PubMed
2 months ago
- Doxorubicin induces ferroptosis in endometrial cancer by suppressing the MKK6/p38/CEBPB axis.
- The study was approved by the Ethics Committee of the Second Affiliated Hospital of Zhengzhou University (Approval No. KY2024200).
- No human participants or human-derived samples were included in the study, so informed consent was not required.
- The authors declare no conflict of interest.
- References include studies on endometrial cancer, global cancer statistics, and real-world outcomes in molecular subgroups for advanced or recurrent endometrial cancer.
In situ delivery of JPH203 via camptothecin-peptide conjugate nanoassemblies to trigger ferroptosis in triple-negative breast cancer - PubMed
2 months ago
- Triple-negative breast cancer (TNBC) lacks druggable targets and resists conventional therapies.
- Ferroptosis, an iron-dependent cell death mechanism, is a promising therapeutic target for TNBC.
- Solute carrier family 7 member 5 (SLC7A5) identified as a ferroptosis-suppressing prognostic target.
- Developed a tumor microenvironment-responsive camptothecin-peptide conjugate (CPC) nanoassembly for in situ JPH203 delivery.
- CPCs feature tumor-targeting motifs, a CPT-based hydrophobic core, and a gelatinase-cleavable linker for controlled release.
- JPH203 blocks leucine uptake, suppresses mTORC1, disrupts iron/redox homeostasis, and induces ferroptosis with 81.2% tumor suppression.
- CPCs-JPH activates dendritic cell maturation and CD8+ T-cell responses, improving survival in TNBC mouse models.
- The nanoplatform combines ferroptosis induction with immune system engagement for enhanced TNBC therapy.
Ironing out COPD: ferroptosis-driven immune dysregulation, metabolic rewiring, and precision therapeutic opportunities - PubMed
2 months ago
- COPD is a global health crisis driven by oxidative stress and immune dysregulation.
- Ferroptosis, an iron-dependent cell death, is a key mediator in COPD pathogenesis.
- Cigarette smoke induces mitochondrial fission, exacerbating ferroptosis in airway epithelial cells.
- Nrf2 signaling's complex role in COPD: suppressed globally but dysfunction in macrophages may promote ferroptosis.
- Plasma malondialdehyde (MDA) serves as a biomarker for oxidative stress severity in COPD.
- Targeted therapeutic strategies like inhaled exosomes with liproxstatin-1 show promise in inhibiting pulmonary ferroptosis.
- The review highlights the ferroptosis-immune axis for precision medicine in COPD.

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#ferroptosis

Persistent PI3K-AKT signaling fortifies cellular defense against oxidative stress and ferroptosis through augmented mitochondrial fitness - PubMed

LINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma - PubMed

Investigating the Mechanism of Rehmannia glutinosa-Ephedra sinica in heart failure with preserved ejection fraction by Network Pharmacology, Metabolomics and Experimental Validation - PubMed

Systemic Integrative Mechanisms and Intervention Strategies in Exercise-Induced Skeletal Muscle Damage: Evidence from Animal, Clinical, and Multi-Omics Studies - PubMed

The interplay between mitophagy and ferroptosis in Alzheimer's disease: Mechanisms and therapeutic implications - PubMed

Human umbilical cord-derived mesenchymal stem cell exosomes ameliorate hepatocyte ferroptosis and sepsis-associated liver injury by restoring iron homeostasis in hepatocytes - PubMed

AURKA-mediated destabilization of SAPS3 drives ferroptosis evasion via 7-dehydrocholesterol biosynthesis in colorectal cancer - PubMed

LCN2 aggravates sepsis-induced ALI by inhibiting MUC1 to activate ER-stress-autophagy induced ferroptosis via lactate/MCT1/AMPK/mTOR axis - PubMed

Traditional Chinese Medicine and Ferroptosis in Alzheimer's Disease: A Potential Therapeutic Approach - PubMed

Insights into the potential pathogenesis and therapeutic implications of ferroptosis in brain microvascular endothelial cells during stroke - PubMed

The hippo-YAP1/TEAD1-SLC7A5 axis: uncovering a novel therapeutic target for oxalate-induced renal tubular ferroptosis - PubMed

Puerarin promotes nerve regeneration and functional recovery after peripheral nerve injury by inhibiting ACSL4-dependent ferroptosis - PubMed

GHRHR Deficiency Enhances Retinal Ganglion Cell Survival and Visual Functions in Experimental Glaucoma by Inhibiting Ferroptosis - PubMed

Chemo-photothermal synergy ignites antitumor immunity via ferroptosis - PubMed

Fisetin alleviates lipopolysaccharide-induced mastitis by inhibiting ferroptosis and modulating the gut microbiota - PubMed

USP20 governs tyrosine kinase inhibitors resistance through ferroptosis evasion by targeting GPX4 in cancers - PubMed

The multifaceted roles of the ACSL family in cancer: Metabolic reprogramming, ferroptosis regulation and tumour immune microenvironment remodelling - PubMed

Doxorubicin induces ferroptosis in endometrial cancer by suppressing the MKK6/p38/CEBPB axis - PubMed

In situ delivery of JPH203 via camptothecin-peptide conjugate nanoassemblies to trigger ferroptosis in triple-negative breast cancer - PubMed

Ironing out COPD: ferroptosis-driven immune dysregulation, metabolic rewiring, and precision therapeutic opportunities - PubMed