Nature Reviews Clinical Oncology, Год журнала: 2023, Номер 21(3), С. 169 - 170
Опубликована: Дек. 6, 2023
Язык: Английский
Trends in Cell Biology, Год журнала: 2025, Номер unknown
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
2
Journal of Molecular Biology, Год журнала: 2024, Номер 436(15), С. 168493 - 168493
Опубликована: Фев. 14, 2024
Protein homeostasis or proteostasis is an equilibrium of biosynthetic production, folding and transport proteins, their timely efficient degradation. Proteostasis guaranteed by a network protein quality control systems aimed at maintaining the proteome functional avoiding accumulation potentially cytotoxic proteins. Terminal unfolded dysfunctional proteins can be directly turned over ubiquitin-proteasome system (UPS) first amassed into aggregates prior to Aggregates also disposed lysosomes selective type autophagy known as aggrephagy, which relies on set so-called receptors (SARs) adaptor Failure in eliminating aggregates, due defects have devastating effects underscored several neurodegenerative diseases proteinopathies, are characterized mostly formed specific disease-associated, aggregate-prone depending clinical pathology. Despite its medical relevance, however, process aggrephagy far from being understood. Here we review findings that helped assigning possible function SARs context highlight interplay between pathogenesis proteinopathies.
Язык: Английский
Процитировано
8
The Journal of Immunology, Год журнала: 2024, Номер 212(11), С. 1807 - 1818
Опубликована: Апрель 19, 2024
Drug-induced acute renal failure (ARF) is a public health concern that hinders optimal drug therapy. However, pathological mechanisms of drug-induced ARF remain to be elucidated. Here, we show process mediated by proinflammatory cross-talk between kidney tubular cells and macrophages. Both polymyxin B colistin, polypeptide antibiotics, frequently cause ARF, stimulated the ERK NF-κB pathways in cells, thereby upregulated M-CSF MCP-1, leading infiltration macrophages into kidneys. Thereafter, kidney-infiltrated were exposed which initiated activation NLR family pyrin domain containing 3 (NLRP3) inflammasome. Interestingly, blockade NLRP3 clearly ameliorated pathology induced suggesting combination distinct cellular responses antibiotics plays key role pathogenesis colistin-induced ARF. Thus, our results provide concrete example how drugs initiate may give insight underlying
Язык: Английский
Процитировано
6
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Год журнала: 2024, Номер 1879(6), С. 189206 - 189206
Опубликована: Ноя. 1, 2024
Язык: Английский
Процитировано
4
Biochemical Pharmacology, Год журнала: 2024, Номер 224, С. 116207 - 116207
Опубликована: Апрель 25, 2024
Язык: Английский
Процитировано
3
Cells, Год журнала: 2024, Номер 13(8), С. 687 - 687
Опубликована: Апрель 15, 2024
Toll-like receptors (TLRs) induce innate immune responses through activation of intracellular signaling pathways, such as MAP kinase and NF-κB play an important role in host defense against bacterial or viral infections. Meanwhile, excessive TLR leads to a variety inflammatory disorders, including autoimmune diseases. is therefore strictly controlled balance optimal response inflammation. However, its balancing mechanisms are not fully understood. In this study, we identified the E3 ubiquitin ligase LINCR/ NEURL3 critical regulator signaling. LINCR-deficient cells, sustained JNK p38 MAPKs induced by agonists for TLR3, TLR4, TLR5, was clearly attenuated. Consistent with these observations, TLR-induced production series cytokines significantly attenuated, suggesting that LINCR positively regulates promoting p38. Interestingly, our further mechanistic study MAPK phosphatase-1 (MKP1), negative kinases, ubiquitination target LINCR. Thus, results demonstrate TLRs fine-tune pathways (the positive regulator) MKP1 regulator), which may contribute induction responses.
Язык: Английский
Процитировано
3
The Journal of Toxicological Sciences, Год журнала: 2025, Номер 50(1), С. 11 - 21
Опубликована: Янв. 1, 2025
A representative surfactant, benzalkonium chloride (BAC) is used as a disinfectant, but sometimes causes serious side effects, including lung disorders such interstitial pneumonia. However, its pathogenic mechanisms remain unexplained. In this study, we identified novel mechanism by which BAC initiates inflammatory responses that may be responsible for effects. We firstly investigated whether inflammation, and found promotes the secretion of pro-inflammatory cytokine interleukin-1β (IL-1β) not tumor necrosis factor-α (TNF-α) in macrophages. Interestingly, IL-1β triggered surfactants was completely blocked K-ATP channel blocker glibenclamide or calcium chelating agent 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA)-AM. Moreover, genetic experiments revealed BAC-dependent mediated NLRP3 inflammasome. These results suggest derangement ion fluxes associated with interfacial effects triggers inflammasome activation subsequent inflammation. Thus, NLRP3-dependent explain pathogenesis surfactant-caused adverse
Язык: Английский
Процитировано
0
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2025, Номер 1871(4), С. 167706 - 167706
Опубликована: Фев. 10, 2025
Язык: Английский
Процитировано
0
Phytomedicine, Год журнала: 2025, Номер 139, С. 156501 - 156501
Опубликована: Фев. 12, 2025
Язык: Английский
Процитировано
0
Advances in experimental medicine and biology, Год журнала: 2025, Номер unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0