Endoplasmic reticulum stress and quality control in relation to cisplatin resistance in tumor cells DOI Creative Commons

Wentao Mu,

Zhi Yao,

Jianpeng Zhou

и другие.

Frontiers in Pharmacology, Год журнала: 2024, Номер 15

Опубликована: Июнь 14, 2024

The endoplasmic reticulum (ER) is a crucial organelle that orchestrates key cellular functions like protein folding and lipid biosynthesis. However, it highly sensitive to disturbances lead ER stress. In response, the unfolded response (UPR) activates restore homeostasis, primarily through three sensors: IRE1, ATF6, PERK. ERAD autophagy are in mitigating stress, yet their dysregulation can accumulation of misfolded proteins. Cisplatin, commonly used chemotherapy drug, induces stress tumor cells, activating complex signaling pathways. Resistance cisplatin stems from reduced drug accumulation, activation DNA repair, anti-apoptotic mechanisms. Notably, cisplatin-induced dualistically affect promoting either survival or apoptosis, depending on context. for degrading proteins, whereas protect cells apoptosis enhance stress-induced apoptosis. interaction between resistance, ERAD, opens new avenues cancer treatment. Understanding these processes could innovative strategies overcome chemoresistance, potentially improving outcomes cisplatin-based treatments. This comprehensive review provides multifaceted perspective mechanisms implications therapy.

Язык: Английский

Lysosomes as coordinators of cellular catabolism, metabolic signalling and organ physiology DOI
Carmine Settembre, Rushika M. Perera

Nature Reviews Molecular Cell Biology, Год журнала: 2023, Номер 25(3), С. 223 - 245

Опубликована: Ноя. 24, 2023

Язык: Английский

Процитировано

95
Protein Misfolding and Aggregation in Proteinopathies: Causes, Mechanism and Cellular Response DOI Creative Commons

Mohammad Ajmal

Diseases, Год журнала: 2023, Номер 11(1), С. 30 - 30

Опубликована: Фев. 9, 2023

Proteins are central to life functions. Alterations in the structure of proteins reflected their function. Misfolded and aggregates present a significant risk cell. Cells have diverse but integrated network protection mechanisms. Streams misfolded that cells continuously exposed must be continually monitored by an elaborated molecular chaperones protein degradation factors control contain misfolding problems. Aggregation inhibition properties small molecules such as polyphenols important they possess other beneficial antioxidative, anti-inflammatory, pro-autophagic help neuroprotection. A candidate with desired features is for any possible treatment development aggregation diseases. There need study phenomenon so we can treat some worst kinds human ailments related aggregation.

Язык: Английский

Процитировано

49
New insights into the role of mitochondrial dynamics in oxidative stress-induced diseases DOI Open Access
Sisi Chen, Qilong Li,

Hanjing Shi

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2024, Номер 178, С. 117084 - 117084

Опубликована: Авг. 1, 2024

The accumulation of excess reactive oxygen species (ROS) can lead to oxidative stress (OS), which induce gene mutations, protein denaturation, and lipid peroxidation directly or indirectly. expression is reduced ATP level in cells, increased cytoplasmic Ca

Язык: Английский

Процитировано

42
Two FAM134B isoforms differentially regulate ER dynamics during myogenesis DOI Creative Commons

Viviana Buonomo,

Kateryna Lohachova, Alessio Reggio

и другие.

The EMBO Journal, Год журнала: 2025, Номер 44(4), С. 1039 - 1073

Опубликована: Янв. 6, 2025

Язык: Английский

Процитировано

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

и другие.

ACS Chemical Neuroscience, Год журнала: 2025, Номер 16(2), С. 223 - 231

Опубликована: Янв. 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.

Язык: Английский

Процитировано

3
TMX4-driven LINC complex disassembly and asymmetric autophagy of the nuclear envelope upon acute ER stress DOI Creative Commons
Marika Kucińska, Juliette Fédry,

Carmela Galli

и другие.

Nature Communications, Год журнала: 2023, Номер 14(1)

Опубликована: Июнь 13, 2023

The endoplasmic reticulum (ER) is an organelle of nucleated cells that produces proteins, lipids and oligosaccharides. ER volume activity are increased upon induction unfolded protein responses (UPR) reduced activation ER-phagy programs. A specialized domain the ER, nuclear envelope (NE), protects cell genome with two juxtaposed lipid bilayers, inner outer membranes (INM ONM) separated by perinuclear space (PNS). Here we report expansion mammalian homeostatic perturbations results in TMX4 reductase-driven disassembly LINC complexes connecting INM ONM swelling. physiologic distance between restored, resolution stress, asymmetric autophagy NE, which involves LC3 lipidation machinery, receptor SEC62 direct capture ONM-derived vesicles degradative LAMP1/RAB7-positive endolysosomes a catabolic pathway mechanistically defined as micro-ONM-phagy.

Язык: Английский

Процитировано

29
The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease DOI Creative Commons
Sarah X. Zhang, Josh J. Wang, Christopher R. Starr

и другие.

Progress in Retinal and Eye Research, Год журнала: 2023, Номер 98, С. 101231 - 101231

Опубликована: Дек. 12, 2023

Язык: Английский

Процитировано

25
Mitophagy in neurodegenerative disease pathogenesis DOI Creative Commons
Kan Yang, Yuqing Yan,

Anni Yu

и другие.

Neural Regeneration Research, Год журнала: 2023, Номер 19(5), С. 998 - 1005

Опубликована: Сен. 22, 2023

Mitochondria are critical cellular energy resources and central to the life of neuron. Mitophagy selectively clears damaged or dysfunctional mitochondria through autophagic machinery maintain mitochondrial quality control homeostasis. Mature neurons postmitotic consume substantial energy, thus require highly efficient mitophagy pathways turn over mitochondria. Recent evidence indicates that is pivotal pathogenesis neurological diseases. However, more work needed study pathway components as potential therapeutic targets. In this review, we briefly discuss characteristics nonselective autophagy selective autophagy, including ERphagy, aggrephagy, mitophagy. We then introduce mechanisms Parkin-dependent Parkin-independent under physiological conditions. Next, summarize diverse repertoire membrane receptors phospholipids mediate Importantly, review role in neurodegenerative diseases Alzheimer's disease, Parkinson's amyotrophic lateral sclerosis. Last, recent studies considering a target for treating Together, our may provide novel views better understand roles disease pathogenesis.

Язык: Английский

Процитировано

23
Sestrin2 drives ER-phagy in response to protein misfolding DOI Creative Commons
Chiara De Leonibus, Marianna Maddaluno, Rosa Ferriero

и другие.

Developmental Cell, Год журнала: 2024, Номер 59(16), С. 2035 - 2052.e10

Опубликована: Авг. 1, 2024

Protein biogenesis within the endoplasmic reticulum (ER) is crucial for organismal function. Errors during protein folding necessitate removal of faulty products. ER-associated degradation and ER-phagy target misfolded proteins proteasomal lysosomal degradation. The mechanisms initiating in response to ER proteostasis defects are not well understood. By studying mouse primary cells patient samples as a model storage disorders (ERSDs), we show that accumulation products triggers involving SESTRIN2, nutrient sensor controlling mTORC1 signaling. SESTRIN2 induction by XBP1 inhibits mTORC1's phosphorylation TFEB/TFE3, allowing these transcription factors enter nucleus upregulate receptor FAM134B along with genes. This promotes via FAM134B-Calnexin complex. Pharmacological improves clearance ERSDs. Our study identifies interplay between signaling quality control, suggesting therapeutic strategies

Язык: Английский

Процитировано

10
The Epstein-Barr virus deubiquitinase BPLF1 regulates stress-induced ribosome UFMylation and reticulophagy DOI Creative Commons
Jiangnan Liu, Noémi Nagy, Carlos Ayala‐Torres

и другие.

Autophagy, Год журнала: 2025, Номер unknown, С. 1 - 23

Опубликована: Янв. 22, 2025

The synthesis of membrane and secreted proteins is safeguarded by an endoplasmic reticulum-associated ribosome quality control (ER-RQC) that promotes the disposal defective translation products proteasome or via a lysosome-dependent pathway involving degradation portions ER macroautophagy (reticulophagy). UFMylation RPL26 on ER-stalled ribosomes essential for activating ER-RQC reticulophagy. Here, we report viral deubiquitinase (vDUB) encoded in N-terminal domain Epstein-Barr virus (EBV) large tegument protein BPLF1 hinders stall at ER, stabilization substrates, inhibits vDUB did not act as de-UFMylase interfere with CYB5R3 UFL1 ligase. Instead, it copurified sucrose gradients abrogated ZNF598- LTN1-independent ubiquitination event required UFMylation. Physiological levels impaired productively EBV-infected cells, pointing to important role enzyme regulating allows efficient production infectious virus.

Язык: Английский

Процитировано

1