An Overview of the Current State of Cell Viability Assessment Methods Using OECD Classification DOI Open Access
Eneko Madorran, Miha Ambrož, Jure Knez

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 26(1), P. 220 - 220

Published: Dec. 30, 2024

Over the past century, numerous methods for assessing cell viability have been developed, and there are many different ways to categorize these accordingly. We chosen use Organisation Economic Co-operation Development (OECD) classification due its regulatory importance. The OECD categorizes into four groups: non-invasive structure damage, invasive growth, cellular metabolism. Despite variety of available, they can all be categorized within groups, except two novel based on membrane potential, which we added list. Each method operates principles has own advantages disadvantages, making it essential researchers choose that best fits their experimental design. This review aims assist in this decision by describing regarding potential providing direct references assessment methods. Additionally, facilitate highlight need adding a new category

Language: Английский

Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions DOI Creative Commons
Megh Pravin Vithalkar, Shaili Pradhan, K. Sandra

et al.

Cell Biochemistry and Biophysics, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 19, 2025

Abstract Idiopathic Pulmonary Fibrosis (IPF) is a severe, rapidly advancing disease that drastically diminishes life expectancy. Without treatment, it can progress to lung cancer. The precise etiology of IPF remains unknown, but inflammation and damage the alveolar epithelium are widely thought be pivotal in its development. Research has indicated activating NLRP3 inflammasome crucial mechanism pathogenesis, as triggers release pro-inflammatory cytokines such IL-1β, IL-18, TGF-β. These contribute myofibroblast differentiation extracellular matrix (ECM) accumulation. Currently, treatment options for limited. Only two FDA-approved medications, pirfenidone nintedanib, available. While these drugs decelerate progression, they come with range side effects do not cure disease. Additional strategies primarily involve supportive care therapy. Emerging research highlighted numerous flavonoids derived from traditional medicines inhibit critical regulators responsible inflammasome. show promise potential therapeutic agents managing IPF, offering new avenue targets core inflammatory processes this debilitating condition. Graphical

Language: Английский

Citations

2
Cuproptosis, ferroptosis and PANoptosis in tumor immune microenvironment remodeling and immunotherapy: culprits or new hope DOI Creative Commons
Xiaojie Zhang, Bufu Tang, Jinhua Luo

et al.

Molecular Cancer, Journal Year: 2024, Volume and Issue: 23(1)

Published: Nov. 15, 2024

Normal life requires cell division to produce new cells, but death is necessary maintain balance. Dysregulation of can lead the survival and proliferation abnormal promoting tumor development. Unlike apoptosis, necrosis, autophagy, newly recognized forms regulated (RCD) cuproptosis, ferroptosis, PANoptosis provide novel therapeutic strategies for treatment. Increasing research indicates that immune cells mediated by these discovered regulate microenvironment (TME) influence effectiveness immunotherapy. This review primarily elucidates molecular mechanisms their complex effects on TME. also summarizes exploration nanoparticle applications in therapy based vivo vitro evidence derived from induction or inhibition RCD pathways.

Language: Английский

Citations

10
PANoptosis in Bacterial Infections: A Double-Edged Sword Balancing Host Immunity and Pathogenesis DOI Creative Commons

Xiaoe He,

Xiangyan Jiang, Jiayin Guo

et al.

Pathogens, Journal Year: 2025, Volume and Issue: 14(1), P. 43 - 43

Published: Jan. 8, 2025

PANoptosis is a newly identified programmed cell death pathway that integrates characteristics of apoptosis, pyroptosis, and necroptosis. It plays dual role in the host immune response to bacterial infections. On one hand, acts as protective mechanism by inducing infected cells eliminate pathogens releasing pro-inflammatory cytokines amplify response. other bacteria can exploit evade defenses. This nature underscores potential target for developing novel therapies against review summarizes molecular mechanisms PANoptosis, along with crosstalk integration different pathways various pathogens. We also discuss roles infectious diseases, including sepsis, pulmonary infections, intestinal Elucidating underlying how manipulate this offers critical insights into host-pathogen interactions. These provide foundation designing targeted antibacterial strategies, modulating inflammation, advancing precision medicine improve clinical outcomes.

Language: Английский

Citations

1
LINC01089 in cancer: multifunctional roles and therapeutic implications DOI Creative Commons

Qiang Yi,

Gangfeng Zhu,

Xinting Ouyang

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: Sept. 27, 2024

Language: Английский

Citations

5
KAE ameliorates LPS-mediated acute lung injury by inhibiting PANoptosis through the intracellular DNA-cGAS-STING axis DOI Creative Commons

Yonghu Chen,

Xilin Wu, Zhe Jiang

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 7, 2025

Acute lung injury (ALI) is a severe condition characterized by inflammation, tissue damage, and persistent activation of the cyclic GMP-AMP (cGAS)-stimulator interferon genes (STING) pathway, which exacerbates production pro-inflammatory mediators promotes progression ALI. Specific inhibition this pathway has been shown to alleviate ALI symptoms. Kaempferol-3-O-α-L-(4″-E-p-coumaroyl)-rhamnoside (KAE), an active compound found in flowers Angelica acutiloba Kitagawa, exhibits anti-inflammatory antioxidant properties. This study aimed investigate molecular mechanisms through KAE regulates cGAS-STING context was induced using LPS. Lung damage anti-inflammatory/antioxidant effects were assessed H&E staining, edema index, SOD, MDA, ELISA assays. NO release mitochondrial membrane potential (MMP) measured JC-1 Griess methods. The impact on PANoptosis analyzed flow cytometry, Western blot, immunofluorescence. significantly alleviated lipopolysaccharide-induced pulmonary reducing inflammatory cell infiltration, alleviating edema, enhancing capacity, decreasing levels cytokines mouse tissues. In both vitro vivo analyses, downregulated expression key components including cGAS, STING, p-TBK1, nuclear factor-κB. also reduced assembly PANoptosome, thereby attenuating apoptosis, necroptosis, pyroptosis. Additionally, inhibited cGAS restoring MMP, cytosolic DNA. improve inhibiting DNA suppressing activation, protecting cells from PANoptosis. Our findings provide valuable insights for development application novel therapeutic strategies

Language: Английский

Citations

0
Unveiling the role of PANoptosis-related genes in breast cancer: an integrated study by multi-omics analysis and machine learning algorithms DOI
Gang Liu,

Liang-Zhi Pan,

Jie Chen

et al.

Breast Cancer Research and Treatment, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 28, 2025

Language: Английский

Citations

0
Multiple programmed cell death patterns predict the prognosis and drug sensitivity in gastric cancer DOI Creative Commons

Qiying Song,

Shihe Liu, Di Wu

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 4, 2025

Background Gastric cancer (GC) is a malignant tumor with poor prognosis. The diverse patterns of programmed cell death (PCD) are significantly associated the pathogenesis and progression GC, it has potential to serve as prognostic drug sensitivity indicators for GC. Method sequencing data clinical characteristics GC patients were downloaded from Cancer Genome Atlas GEO databases. LASSO cox regression method was used screen feature genes develop PCD score (PCDS). Immune infiltration, immune checkpoint expression, Tumor Dysfunction Exclusion (TIDE) algorithm analysis explore immunotherapy response. By integrating PCDS characteristics, we constructed validated nomogram that demonstrated robust predictive performance. Results We screened nine PCD-related (SERPINE1, PLPPR4, CDO1, MID2, NOX4, DYNC1I1, PDK4, MYB, TUBB2A) create PCDS. found high experienced poorer prognoses, identified an independent factor. Furthermore, there significant difference in profile between low groups. Additionally, indicated may exhibit resistance standard adjuvant chemotherapy regimens; however, they benefit FDA-approved Dasatinib. Conclusion Overall, confirmed risk factor valuable predictor response patients, which provides new evidence application

Language: Английский

Citations

0
Dkk3 inhibits the aggressiveness and mitigates chemoresistance through low lipid droplet formation in gastric cancer: A biomarker and gene therapy target DOI

R Liu,

Guoliang Zheng, Ning Li

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 149, P. 114200 - 114200

Published: Feb. 4, 2025

Language: Английский

Citations

0
The Interplay of Aging and PANoptosis in Osteoarthritis Pathogenesis: Implications for Novel Therapeutic Strategies DOI Creative Commons

Shaoshan Liu,

Guifeng Zhang, Nan Li

et al.

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 1951 - 1967

Published: Feb. 1, 2025

Abstract: Osteoarthritis (OA) is a common degenerative joint disease characterized by the progressive degradation of articular cartilage, synovial inflammation, and subchondral bone remodeling. This review explores interplay between aging, PANoptosis, inflammation in OA progression. Age-related cellular immune dysfunctions, including senescence, senescence-associated secretory phenotypes (SASPs), immunosenescence, significantly contribute to degeneration. In OA, dysregulated apoptosis, necroptosis, pyroptosis, particularly chondrocytes, exacerbate cartilage damage. Apoptosis, mediated JNK pathway, reduces chondrocyte density, while necroptosis involving RIPK-1/RIPK-3 NLRP3 inflammasome, respectively, amplify destruction. Inflammatory cytokines damage-associated molecular patterns (DAMPs) further enhance these PANoptotic pathways. Current therapeutic strategies primarily focus on anti-inflammatory agents such as non-steroidal drugs (NSAIDs) corticosteroids, with growing interest anti-senescence targeting senescence SASP. Additionally, exploring PANoptosis mechanisms offers potential for innovative treatments. Keywords: osteoarthritis,

Language: Английский

Citations

0
Fullerenols hijack lysosomes to disrupt inter-organellar crosstalk and block autophagy pre-activated by mTOR inhibitors for cancer cell PANoptosis DOI Creative Commons
Hedong Qi, Xue Li, Jing Ma

et al.

Science Bulletin, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Subcellular inter-organellar crosstalk among lysosome, endoplasmic reticulum (ER), and mitochondrion is crucial for cancer cell survival a promising target in treatment; however, efficiently disrupting these interactive networks challenging. Herein, communication interception strategy presented, which specifically disrupts by lysosomal contents leakage along with their trajectory pre-activates autophagic flux to augment the lysosome-associated autophagy blocking preventing self-repair of this subcellular disorder. Briefly, fullerenols containing multiple hydroxyl groups (MF) tear phospholipid membrane through direct interaction, causes (calcium ions cathepsins) leak into cytoplasm, subsequently leading stress mitochondrial dysfunction redox imbalance metabolic reprogramming. mTOR inhibitors activate amplify autophagy, then impaired lysosomes prevent fusion autophagosome, thus paralyzed autolysosome accumulation. Consequently, cellular homeostasis compromised destroyed without thereby triggering PANoptotic processes remarkable anti-tumor therapeutic efficacy vitro vivo. This demonstrates selective cytotoxicity non-toxic nanomaterials that interfere crosstalk, offering novel method designing tumor therapies.

Language: Английский

Citations

0