Podocyte programmed cell death in diabetic kidney disease: Molecular mechanisms and therapeutic prospects DOI Open Access

Haoyu Yang,

Jun Sun,

Aru Sun

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 177, P. 117140 - 117140

Published: July 16, 2024

Language: Английский

Cuproptosis: molecular mechanisms, cancer prognosis, and therapeutic applications DOI Creative Commons
Y. Cong, Na Li, Zixin Zhang

et al.

Journal 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

4

Heterogeneous ferroptosis susceptibility of macrophages caused by focal iron overload exacerbates rheumatoid arthritis DOI Creative Commons
Yan Liu,

Xiqing Luo,

Ye Chen

et al.

Redox Biology, Journal Year: 2023, Volume and Issue: 69, P. 103008 - 103008

Published: Dec. 20, 2023

Focal iron overload is frequently observed in patients with rheumatoid arthritis (RA), yet its functional significance remains elusive. Herein, we report that deposition lesion aggravates by inducing macrophage ferroptosis. We show excessive synovial fluid positively correlates RA disease severity as does lipid hyperoxidation of focal monocyte/macrophages. Further study reveals high susceptibility to induced ferroptosis the anti-inflammatory macrophages M2, while pro-inflammatory M1 are less affected. Distinct glutathione peroxidase 4 (GPX4) degradation depending on p62/SQSTM1 two cell types make great contribution mechanically. Of note, inhibitor liproxstatin-1 (LPX-1) can alleviate progression K/BxN serum-transfer (STIA) mice accompanied increasing M2 proportion. thus propose heterogeneous subtypes well consequent inflammation and immune disorders potential biomarkers therapeutic targets RA.

Language: Английский

Citations

24

The role of competing endogenous RNA network in the development of hepatocellular carcinoma: potential therapeutic targets DOI Creative Commons
Ziwei Tang, Xue Li,

Yanfeng Zheng

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Jan. 31, 2024

The current situation of hepatocellular carcinoma (HCC) management is challenging due to its high incidence, mortality, recurrence and metastasis. Recent advances in gene genetic expression regulation have unveiled the significant role non-coding RNA (ncRNA) various cancers. This led formulation competing endogenous (ceRNA) hypothesis, which posits that both coding ncRNA, containing miRNA response elements (MRE), can share same sequence. results a competitive network between ncRNAs, such as lncRNA mRNA, allowing them regulate each other. Extensive research has highlighted crucial ceRNA HCC development, impacting cellular processes including proliferation, metastasis, cell death, angiogenesis, tumor microenvironment, organismal immunity, chemotherapy resistance. Additionally, network, mediated by or circRNA, offers potential early diagnosis prevention HCC. Consequently, ceRNAs are emerging therapeutic targets for complexity these networks aligns with multi-target approach traditional Chinese medicine (TCM), presenting novel perspective TCM combating Research beginning show compounds prescriptions affect progression through inhibiting proliferation inducing apoptosis. Currently, lncRNAs TUG1, NEAT1, CCAT1, along their associated networks, among most promising ncRNAs research. However, this field still infancy, necessitating advanced technology extensive basic fully understand mechanisms treatment.

Language: Английский

Citations

15

Entosis: the core mechanism and crosstalk with other cell death programs DOI Creative Commons
Sung-Hoon Kim, Donghyuk Lee, Sung Eun Kim

et al.

Experimental & Molecular Medicine, Journal Year: 2024, Volume and Issue: 56(4), P. 870 - 876

Published: April 2, 2024

Abstract Cell death pathways play critical roles in organism development and homeostasis as well the pathogenesis of various diseases. While studies over last decade have elucidated numerous different forms cell that can eliminate cells contexts, how certain mechanisms impact physiology is still not understood. Moreover, recent shown multiple occur a population, with eliminating individual cells. Here, we aim to describe known molecular entosis, non-apoptotic engulfment process, discuss signaling control its induction possible crosstalk other mechanisms.

Language: Английский

Citations

13

Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases DOI
Zhibo Yang,

Ridong Feng,

Zhao Hai

et al.

APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(9-10), P. 1330 - 1360

Published: July 16, 2024

Language: Английский

Citations

12

Cell death in cancer chemotherapy using taxanes DOI Creative Commons

Ana P. Xu,

Lucy B. Xu,

Elizabeth R. Smith

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 14

Published: Jan. 5, 2024

Cancer cells evolve to be refractory the intrinsic programmed cell death mechanisms, which ensure cellular tissue homeostasis in physiological conditions. Chemotherapy using cytotoxic drugs seeks eliminate cancer but spare non-cancerous host by exploring a likely subtle difference between malignant and benign cells. Presumably, chemotherapy agents achieve efficacy triggering machineries Currently, many major solid tumors are treated with composed of combination platinum taxanes. Platinum agents, largely cis-platin, carboplatin, oxaliplatin, DNA damaging that covalently form addicts, repair response pathways. Taxanes, including paclitaxel, docetaxel, cabazitaxel, microtubule stabilizing often very effective purging clinical settings. Generally, it is thought stabilization microtubules taxanes leads mitotic arrest, catastrophe, apoptotic death. However, precise mechanism(s) how arrest catastrophe activate caspase pathway has not been established. Here, we briefly review literature on involvement potential mechanisms therapy. These include classical caspase-mediated death, necroptosis mediated MLKL, pore forming immune cells, etc. In particular, discuss newly recognized mechanism taxane-treatment involves micronucleation irreversible rupture nuclear membrane. Since commonly retarded responding signaling, stabilized bundle-induced membrane rupture, rather than apoptosis, may key accounting for success as anti-cancer agents.

Language: Английский

Citations

10

Arnicolide D induces endoplasmic reticulum stress-mediated oncosis via ATF4 and CHOP in hepatocellular carcinoma cells DOI Creative Commons
Yu-Shan Lin,

Zhiwei Sun,

Lisha Shen

et al.

Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: March 12, 2024

Abstract Endoplasmic reticulum (ER) stress can trigger various cell death mechanisms beyond apoptosis, providing promise in cancer treatment. Oncosis, characterized by cellular swelling and increased membrane permeability, represents a non-apoptotic form of death. In our study, we discovered that Arnicolide D (AD), natural sesquiterpene lactone compound, induces ER stress-mediated oncosis hepatocellular carcinoma (HCC) cells, this process is reactive oxygen species (ROS)-dependent. Furthermore, identified the activation PERK-eIF2α-ATF4-CHOP pathway during as pivotal factor AD-induced oncosis. Notably, protein synthesis inhibitor cycloheximide (CHX) was found to effectively reverse oncosis, suggesting ATF4 CHOP may hold crucial roles induction AD. These proteins play vital part promoting stress, ultimately leading Subsequent studies, where individually or simultaneously knocked down HCC provided further confirmation their indispensable Moreover, additional animal experiments not only substantiated AD’s ability inhibit tumor growth but also solidified essential role ROS-dependent therapeutic potential. summary, research findings strongly indicate AD holds agent for its induce

Language: Английский

Citations

10

Programmed cell death in tumor immunity: mechanistic insights and clinical implications DOI Creative Commons

Man Wang,

Fei Yu, Yuan Zhang

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 14

Published: Jan. 12, 2024

Programmed cell death (PCD) is an evolutionarily conserved mechanism of suicide that controlled by various signaling pathways. PCD plays important role in a multitude biological processes, such as turnover, development, tissue homeostasis and immunity. Some forms PCD, including apoptosis, autophagy-dependent death, pyroptosis, ferroptosis necroptosis, contribute to carcinogenesis cancer thus have attracted increasing attention the field oncology. Recently, research-based evidence has demonstrated acts critical modulator tumor can affect function innate adaptive immune cells, which leads distinct immunological consequences, priming tumor-specific T immunosuppression evasion. Targeting alone or combination with conventional immunotherapy may provide new options enhance clinical efficacy anticancer therapeutics. In this review, we introduce characteristics mechanisms ubiquitous pathways (e.g., pyroptosis ferroptosis) explore complex interaction between these immunity based on currently available evidence. We also discuss therapeutic potential PCD-based approaches outlining trials targeting treatment. Elucidating immune-related effects pathogenesis will likely improved understanding oncoimmunology allow be exploited for

Language: Английский

Citations

9

Tetramethylpyrazine attenuates renal tubular epithelial cell ferroptosis in contrast-induced nephropathy by inhibiting transferrin receptor and intracellular reactive oxygen species DOI Creative Commons

Zhongqiang Zhu,

Jun Li, Zhiyong Song

et al.

Clinical Science, Journal Year: 2024, Volume and Issue: 138(5), P. 235 - 249

Published: Feb. 15, 2024

Abstract Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury (AKI). Recently, ferroptosis was reported to be crucial for AKI pathogenesis. Our previous studies indicated antioxidant tetramethylpyrazine (TMP) prevent CIN in vivo. However, whether involved TMP nephroprotective mechanism against unclear. In the present study, we investigated role renal tubular epithelial cell reno-protective effect and molecular mechanisms by which regulates ferroptosis. Classical contrast-medium, Iohexol, used construct models rats HK-2 cells. Results showed that accompanied both vivo vitro, including typical features ferroptosis, Fe2+ accumulation, lipid peroxidation decreased glutathione peroxidase 4 (GPX4). Ferroptosis inhibition classic inhibitors Fer-1 DFO promoted viability reduced intracellular ROS production. Additionally, significantly inhibited dysfunction, biomarkers, prevented production, accumulation increased GPX4 expression. Expressions various proteins associated with iron ion metabolism, transferrin receptor (TFRC), divalent metal transporter 1, iron-responsive element binding protein 2, ferritin heavy chain ferroportin heat shock factor were examined using mechanistic analyses. Among these, TFRC changes most significant after pretreatment. siRNA knockdown plasmid overexpression essential alleviate reduce LDH release, ROS. findings provide insights about potential treating

Language: Английский

Citations

9

Programmed cell death in hepatocellular carcinoma: mechanisms and therapeutic prospects DOI Creative Commons

Xiang’an Wu,

Jingying Cao,

Xueshuai Wan

et al.

Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: Aug. 8, 2024

Hepatocellular Carcinoma (HCC), the most common primary liver cancer, ranks as third cause of cancer-related deaths globally. A deeper understanding cell death mechanisms in HCC is essential for developing more effective treatment strategies. This review explores programmed (PCD) pathways involved HCC, including apoptosis, necroptosis, pyroptosis, ferroptosis, and immunogenic (ICD). These trigger specific cascades that influence development progression HCC. Although multiple PCD are shared cellular factors suggest a possible interplay between different forms death. However, exact roles which pathway plays major role remain unclear. also highlights how disruptions related to drug resistance cancer therapy, promoting combined approach induction anti-tumor enhance therapeutic efficacy. Further research required unravel complex modalities may lead innovative breakthroughs.

Language: Английский

Citations

9