Crosstalk Between Autophagy and Other Forms of Programmed Cell Death DOI Creative Commons
Huaiyuan Wang, Xu Feng, Huilin He

et al.

European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: 995, P. 177414 - 177414

Published: Feb. 20, 2025

Cell death occurs continuously throughout individual development. By removing damaged or senescent cells, cell not only facilitates morphogenesis during the developmental process, but also contributes to maintaining homeostasis after birth. In addition, reduces spread of pathogens by eliminating infected cells. is categorized into two main forms: necrosis and programmed death. Programmed encompasses several types, including autophagy, pyroptosis, apoptosis, necroptosis, ferroptosis, PANoptosis. Autophagy, a mechanism that maintains cellular equilibrium via breakdown reutilization proteins organelles, implicated in regulating almost all forms pathological contexts. Notably, PANoptosis are directly classified as autophagy-mediated Therefore, autophagy presents therapeutic approach for treating diseases such inflammation tumors arise from abnormalities other This review focuses on crosstalk between modalities, providing new perspectives clinical interventions inflammatory neoplastic diseases.

Language: Английский

Mechanism of Decision Making between Autophagy and Apoptosis Induction upon Endoplasmic Reticulum Stress DOI Open Access
Orsolya Kapuy

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(8), P. 4368 - 4368

Published: April 15, 2024

Dynamic regulation of the cellular proteome is mainly controlled in endoplasmic reticulum (ER). Accumulation misfolded proteins due to ER stress leads activation unfolded protein response (UPR). The primary role UPR reduce bulk damages and try drive back system former or a new homeostatic state by autophagy, while an excessive level results apoptosis. It has already been proven that proper order characteristic features both surviving self-killing mechanisms are negative positive feedback loops, respectively. suggest these loops found not only within but also between branches UPR, fine-tuning stress. In this review, we summarize recent knowledge dynamical mechanism using theoretical molecular biological techniques. addition, review pays special attention describing action controlling life-and-death decision upon Since appears diseases common worldwide, more detailed understanding behaviour medical importance.

Language: Английский

Citations

22
Copper exposure induces mitochondrial dysfunction and hepatotoxicity via the induction of oxidative stress and PERK/ATF4 -mediated endoplasmic reticulum stress DOI
Meng Li, Shusheng Tang, Tony Velkov

et al.

Environmental Pollution, Journal Year: 2024, Volume and Issue: 352, P. 124145 - 124145

Published: May 10, 2024

Language: Английский

Citations

21
Elevating VAPB-PTPIP51 integration repairs damaged mitochondria-associated endoplasmic reticulum membranes and inhibits lung fibroblasts activation DOI

Jiaqi Ban,

Hongru Tian,

Yungeng Wei

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 147, P. 113982 - 113982

Published: Jan. 5, 2025

Language: Английский

Citations

4
Oxidative Stress and Reprogramming of Lipid Metabolism in Cancers DOI Creative Commons
Siqi Li, Hang Yuan, Liang Li

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 201 - 201

Published: Feb. 10, 2025

Oxidative stress is a common event involved in cancer pathophysiology, frequently accompanied by unique lipid metabolic reprogramming phenomena. caused mainly an imbalance between the production of reactive oxygen species (ROS) and antioxidant system cells. Emerging evidence has reported that oxidative regulates expression activity metabolism-related enzymes, leading to alteration cellular metabolism; this involves significant increase fatty acid synthesis shift way which lipids are taken up utilized. The dysregulation metabolism provides abundant intermediates synthesize biological macromolecules for rapid proliferation cells; moreover, it contributes maintenance intracellular redox homeostasis producing variety reducing agents. Moreover, derivatives metabolites play critical roles signal transduction within cells tumor microenvironment evades immune destruction facilitates invasion metastasis. These findings suggest close relationship during malignant progression cancers. This review focuses on crosstalk reprogramming, in-depth insight into modulation ROS cancers discusses potential strategies targeting therapy.

Language: Английский

Citations

4
Dual-Enzyme-Instructed Peptide Self-Assembly to Boost Immunogenic Cell Death by Coordinating Intracellular Calcium Overload and Chemotherapy DOI
H. H. Zhang, Yuhan Hu,

Yinghao Ding

et al.

ACS Nano, Journal Year: 2025, Volume and Issue: 19(1), P. 488 - 503

Published: Jan. 4, 2025

The concept of immunogenic cell death (ICD) induced by chemotherapy as a potential synergistic modality for cancer immunotherapy has been widely discussed. Unfortunately, most chemotherapeutic agents failed to dictate effective ICD responses due their defects in inducing potent signaling. Here, we report dual-enzyme-instructed peptide self-assembly platform CPMC (CPT-GFFpY-PLGVRK-Caps) that cooperatively utilizes camptothecin (CPT) and capsaicin (Caps) promote engage systemic adaptive immunity tumor rejection. Although CPT Caps respectively prevent progression inhibiting type-I DNA topoisomerase activating transient receptor cation channel subfamily V member 1 (TRPV1) intracellular calcium overload, neither alone effectively stimulates sufficient signaling meet immunotherapeutic needs. CPMC, sequentially allowing an active derivative VRK-Caps release extracellularly intracellularly, can synergize two distinct apoptosis pathways stimulated increase immunogenicity elicit T-cell-based immunity. Consequently, facilitates the generation improved tumor-specific cytotoxic T-cell sustained immunological memory, successfully suppressing both primary distant tumors. Moreover, render tumors susceptible PD-L1 blockade with antiprogrammed death-ligand (aPDL1) antibody inhibition. Combining drugs low ICD-stimulating capacity using strategy was demonstrated boost potentiate immunotherapy.

Language: Английский

Citations

3
Visualizing Endoplasmic Reticulum Stress and Autophagy in Alzheimer’s Model Cells by a Peroxynitrite-Responsive AIEgen Fluorescent Probe DOI

Lushan Huang,

Liyi Ma,

Qunyan Zhu

et al.

ACS Chemical Neuroscience, Journal Year: 2025, Volume and Issue: 16(2), P. 223 - 231

Published: Jan. 7, 2025

Endoplasmic reticulum (ER) stress and autophagy (ER-phagy) occurring in nerve cells are crucial physiological processes closely associated with Alzheimer's disease (AD). Visualizing the two is paramount to advance our understanding of AD pathologies. Among biomarkers identified, peroxynitrite (ONOO-) emerges as a key molecule initiation aggravation ER ER-phagy, highlighting its significance underlying mechanisms processes. In this work, we designed synthesized an innovative ONOO--responsive AIEgen-based fluorescent probe (DHQM) ability monitor ER-phagy model cells. DHQM demonstrated excellent aggregation-induced emission (AIE) properties, endowing it outstanding for washing-free intracellular imaging. Meanwhile, exhibited high sensitivity, remarkable selectivity ONOO-, exceptional ER-targeting ability. The was successfully applied fluorescence imaging ONOO- fluctuations assess status aluminum-induced Our findings revealed that ferroptosis, regulated cell death process, pivotal excessive production, which turn activated exacerbated stress. Furthermore, aluminum-stimulated observed utilizing DHQM, might be inhibiting ferroptosis mitigating aberrant Overall, study not only offers valuable insights into pathological at level but also opens new potential therapeutic avenues targeting these pathways.

Language: Английский

Citations

3
Shared signaling pathways and comprehensive therapeutic approaches among diabetes complications DOI Creative Commons
Moein Ebrahimi, Hamid Ahmadieh, Mozhgan Rezaei Kanavi

et al.

Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 11

Published: Jan. 8, 2025

The growing global prevalence of diabetes mellitus (DM), along with its associated complications, continues to rise. When clinically detected most DM complications are irreversible. It is therefore crucial detect and address these early systematically in order improve patient care outcomes. current clinical practice often prioritizes by addressing one complication while overlooking others that could occur. proposed the commonly targeted cell types including vascular cells, immune glial fibroblasts mediate might share responses diabetes. In addition, impact be influenced other complications. Recognizing focusing on shared among impacted cellular constituents, will allow simultaneously all DM-related limit adverse treatment impacts. This review explores understanding pathological signaling mechanisms recognizes new concepts benefit from further investigation both basic settings. ultimate goal develop more comprehensive strategies, which effectively multiple organs

Language: Английский

Citations

3
Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions DOI Creative Commons
И. Ф. Беленичев, Olena Popazova, Nina Bukhtiyarova

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 108 - 108

Published: Jan. 18, 2025

The study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation reactive oxygen species (ROS), calcium homeostasis, and execution apoptotic processes. Disruptions function, driven by factors such as oxidative stress, excitotoxicity, altered ion balance, lead to neuronal death contribute cognitive impairments several brain diseases. Mitochondrial can arise from genetic mutations, ischemic events, hypoxia, other environmental factors. This article highlights critical role progression diseases discusses need targeted therapeutic strategies attenuate damage, restore enhance neuroprotection.

Language: Английский

Citations

3
Co-Exposure to Ammonia and Lipopolysaccharide-Induced Impaired Energy Metabolism via the miR-1599/HK2 Axis and Triggered Autophagy, ER Stress, and Apoptosis in Chicken Cardiomyocytes DOI Creative Commons

Zhiyu Hao,

Minna Qiu,

Yuhao Liu

et al.

Poultry Science, Journal Year: 2025, Volume and Issue: 104(4), P. 104965 - 104965

Published: March 1, 2025

Ammonia (NH3) and lipopolysaccharide (LPS), common pollutants in poultry farming environments, pose significant health risks by disrupting cellular processes. Although previous studies have demonstrated the individual effect of NH3 or LPS on human animal health, mechanisms underlying their combined impact chicken heart tissue remain poorly understood. In this study, we established a cardiotoxicity model to investigate effects and/or exposure energy metabolism, autophagy, endoplasmic reticulum (ER) stress, apoptosis cardiomyocytes. Our findings indicated that or/and reduced ATPase activity ATP content, led downregulation HK2, PK, PDHX, SDH, upregulation AMPK, resulting impaired metabolism Additionally, found gga-miR-1599/HK2 axis as key regulator involved LPS-induced impairment. The impairment activated AMPK/mTOR pathway, which subsequently triggered evidenced Beclin, LC3-I, LC3-II. Furthermore, decreased mTOR expression induced ER markers such ATF6, GRP78, IRE1, PERK. turn, increased CHOP expression, downregulated Bcl-2 upregulated Bim, elevated levels Bax, caspase-9, caspase-3, ultimately triggering apoptosis. This study provides valuable insights into co-exposure identifies potential molecular targets for mitigating these adverse effects.

Language: Английский

Citations

3
The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease DOI Creative Commons
Sarah X. Zhang, Josh J. Wang, Christopher R. Starr

et al.

Progress in Retinal and Eye Research, Journal Year: 2023, Volume and Issue: 98, P. 101231 - 101231

Published: Dec. 12, 2023

Language: Английский

Citations

29