A Forward Vision for Chemodynamic Therapy: Issues and Opportunities DOI
Peiran Zhao, Huiyan Li, Wenbo Bu

и другие.

Angewandte Chemie International Edition, Год журнала: 2023, Номер 62(7)

Опубликована: Янв. 17, 2023

Abstract Since the insight to fuse Fenton chemistry and nanomedicine into cancer therapy, great signs of progress have been made in field chemodynamic therapy (CDT). However, exact mechanism CDT is obscured by unique tumor chemical environment inevitable nanoparticle‐cell interactions, thus impeding further development. In this Scientific Perspective, significance clarified, complex deconstructed primitive biological research directions based on kinetics signaling pathways are discussed detail. Moreover, beneficial outlooks presented enlighten evolution next‐generation CDT. Hopefully, Perspective can inspire new ideas advances for provide a reference breaking down interdisciplinary barriers nanomedicine.

Язык: Английский

Proteasomal and Autophagic Degradation Systems DOI Open Access
Ivan Ðikić

Annual Review of Biochemistry, Год журнала: 2017, Номер 86(1), С. 193 - 224

Опубликована: Май 1, 2017

Autophagy and the ubiquitin-proteasome system are two major quality control pathways responsible for cellular homeostasis. As such, they provide protection against age-associated changes a plethora of human diseases. Ubiquitination is utilized as degradation signal by both systems, albeit in different ways, to mark cargoes proteasomal lysosomal degradation. Both systems intersect communicate at multiple points coordinate their actions proteostasis organelle This review summarizes molecular details how proteasome autophagy functionally interconnected cells indicates common principles nodes communication that can be therapeutically exploited.

Язык: Английский

Процитировано

970

Autophagy during viral infection — a double-edged sword DOI Open Access
Younho Choi,

James W. Bowman,

Jae U. Jung

и другие.

Nature Reviews Microbiology, Год журнала: 2018, Номер 16(6), С. 341 - 354

Опубликована: Март 19, 2018

Язык: Английский

Процитировано

668

Proteostasis control by the unfolded protein response DOI
Claudio Hetz, Éric Chevet, Scott A. Oakes

и другие.

Nature Cell Biology, Год журнала: 2015, Номер 17(7), С. 829 - 838

Опубликована: Июнь 30, 2015

Язык: Английский

Процитировано

657

Acute Kidney Injury DOI Open Access
Anna Żuk, Joseph V. Bonventre

Annual Review of Medicine, Год журнала: 2016, Номер 67(1), С. 293 - 307

Опубликована: Янв. 14, 2016

Acute kidney injury (AKI) is a global public health concern associated with high morbidity, mortality, and healthcare costs. Other than dialysis, no therapeutic interventions reliably improve survival, limit injury, or speed recovery. Despite recognized shortcomings of in vivo animal models, the underlying pathophysiology AKI its consequence, chronic disease (CKD), rich biological targets. We review recent findings relating to renal vasculature cellular stress responses, primarily intersection unfolded protein response, mitochondrial dysfunction, autophagy, innate immune response. Maladaptive repair mechanisms that persist following acute phase promote inflammation fibrosis phase. Here macrophages, growth-arrested tubular epithelial cells, endothelium, surrounding pericytes are key players progression disease. Better understanding these complex interacting pathophysiological mechanisms, their relative importance humans, utility biomarkers will lead strategies prevent treat impede CKD end-stage (ESRD).

Язык: Английский

Процитировано

634

New insights into the interplay between autophagy, gut microbiota and inflammatory responses in IBD DOI Creative Commons

Anaïs Larabi,

Nicolas Barnich, Hang Thi Thu Nguyen

и другие.

Autophagy, Год журнала: 2019, Номер 16(1), С. 38 - 51

Опубликована: Июль 9, 2019

One of the most significant challenges inflammatory bowel disease (IBD) research is to understand how alterations in symbiotic relationship between genetic composition host and intestinal microbiota, under impact specific environmental factors, lead chronic inflammation. Genome-wide association studies, followed by functional have identified a role for numerous autophagy genes IBD, especially Crohn disease. Studies using vitro vivo models, addition human clinical studies revealed that pivotal homeostasis maintenance, gut ecology regulation, appropriate immune responses anti-microbial protection. This review describes latest researches on mechanisms which dysfunctional leads disrupted epithelial function, dysbiosis, defect peptide secretion Paneth cells, endoplasmic reticulum stress response aberrant pathogenic bacteria. A better understanding IBD pathogenesis may provide sub-classification phenotypes novel approaches management.Abbreviations: AIEC: adherent-invasive Escherichia coli; AMPK: AMP-activated protein kinase; ATF6: activating transcription factor 6; ATG: related; Atg16l1[ΔIEC] mice: mice with Atg16l1 depletion specifically cells; Atg16l1[HM] hypomorphic expression; BCL2: B cell leukemia/lymphoma 2; BECN1: beclin 1, CALCOCO2: calcium binding coiled-coil domain CASP: caspase; CD: disease; CGAS: cyclic GMP-AMP synthase; CHUK/IKKA: conserved helix-loop-helix ubiquitous CLDN2: claudin DAPK1: death associated kinase 1; DCs: dendritic DSS: dextran sulfate sodium; EIF2A: eukaryotic translation initiation 2A; EIF2AK: 2 alpha ER: reticulum; ERBIN: Erbb2 interacting protein; ERN1/IRE1A: ER nucleus signaling FNBP1L: formin 1-like; FOXP3: forkhead box P3; GPR65: G-protein coupled receptor 65; GSK3B: glycogen synthase 3 beta; IBD: IECs: IFN: interferon; IL: interleukin; IL10R: interleukin 10 receptor; IRGM: immunity related GTPase M; ISC: stem cell; LAMP1: lysosomal-associated membrane LAP: LC3-associated phagocytosis; MAP1LC3B: microtubule-associated 1 light chain LPS: lipopolysaccharide; LRRK2: leucine-rich repeat MAPK: mitogen-activated MHC: major histocompatibility complex; MIF: macrophage migration inhibitory factor; MIR/miRNA: microRNA; MTMR3: myotubularin 3; MTOR: mechanistic target rapamycin MYD88: myeloid differentiation primary gene 88; NLRP3: NLR family, pyrin containing NOD2: nucleotide-binding oligomerization NPC: Niemann-Pick type C; NPC1: NPC intracellular cholesterol transporter OMVs: outer vesicles; OPTN: optineurin; PI3K: phosphoinositide 3-kinase; PRR: pattern-recognition PTPN2: tyrosine phosphatase, non-receptor PTPN22: 22 (lymphoid); PYCARD/ASC: PYD CARD containing; RAB2A: RAB2A, member RAS oncogene family; RELA: v-rel reticuloendotheliosis viral homolog (avian); RIPK2: (TNFRSF)-interacting serine-threonine ROS: reactive oxygen species; SNPs: single nucleotide polymorphisms; SQSTM1: sequestosome TAX1BP1: Tax1 Th: T helper TIRAP/TRIF: toll-interleukin (TIR) domain-containing adaptor TLR: toll-like TMEM173/STING: transmembrane 173; TMEM59: 59; TNF/TNFA: tumor necrosis Treg: regulatory T; TREM1: triggering expressed cells UC: ulcerative colitis; ULK1: unc-51 like WT: wild-type; XBP1: X-box XIAP: X-linked inhibitor apoptosis.

Язык: Английский

Процитировано

625

Quality Control in the Endoplasmic Reticulum: Crosstalk between ERAD and UPR pathways DOI
Jiwon Hwang, Ling Qi

Trends in Biochemical Sciences, Год журнала: 2018, Номер 43(8), С. 593 - 605

Опубликована: Июнь 29, 2018

Язык: Английский

Процитировано

464

Ubiquitin ligases in oncogenic transformation and cancer therapy DOI
Daniela Senft, Jianfei Qi, Ze’ev A. Ronai

и другие.

Nature reviews. Cancer, Год журнала: 2017, Номер 18(2), С. 69 - 88

Опубликована: Дек. 15, 2017

Язык: Английский

Процитировано

407

Cancer and ER stress: Mutual crosstalk between autophagy, oxidative stress and inflammatory response DOI Open Access
Yu‐Ning Lin, Mei Jiang, Wanjun Chen

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2019, Номер 118, С. 109249 - 109249

Опубликована: Июль 24, 2019

The endoplasmic reticulum (ER) acts as a moving organelle with many important cellular functions. As the ER lacks sufficient nutrients under pathological conditions leading to uncontrolled protein synthesis, aggregation of unfolded/misfolded proteins in lumen causes unfolded response (UPR) be activated. Chronic stress produces endogenous or exogenous damage cells and activates UPR, which leads impaired intracellular calcium redox homeostasis. UPR is capable recognizing accumulation ER. enhances ability fold apoptosis when function fails return normal. In different malignancies, can effectively induce occurrence autophagy because malignant tumor need re-use their organelles maintain growth. Autophagy simultaneously counteracts stress-induced expansion has effect enhancing cell viability non-apoptotic death. Oxidative also affects mitochondrial through overload. Mitochondrial reactive oxygen species (ROS) are produced by calcium-enhanced release. toxic substances mitochondria destroys basic function. It known that sustained trigger an inflammatory pathway. Inflammatory thought associated development. This review discusses emerging links between responses autophagy, oxidative stress, signals well potential development targeting this multifaceted signaling pathway various cancers.

Язык: Английский

Процитировано

392

Autophagy as a molecular target for cancer treatment DOI
Nur Mehpare Kocatürk, Yunus Akkoç, Cenk Kığ

и другие.

European Journal of Pharmaceutical Sciences, Год журнала: 2019, Номер 134, С. 116 - 137

Опубликована: Апрель 11, 2019

Язык: Английский

Процитировано

343

Mitochondrial quality control in kidney injury and repair DOI
Chengyuan Tang, Juan Cai,

Xiao-Ming Yin

и другие.

Nature Reviews Nephrology, Год журнала: 2020, Номер 17(5), С. 299 - 318

Опубликована: Ноя. 24, 2020

Язык: Английский

Процитировано

338