The Mechanism of Acupuncture Regulating Autophagy: Progress and Prospect DOI Creative Commons

Jing He,

Min He, Mengmeng Sun

et al.

Biomolecules, Journal Year: 2025, Volume and Issue: 15(2), P. 263 - 263

Published: Feb. 11, 2025

Autophagy plays a crucial role in the physiopathological mechanisms of diseases by regulating cellular functions and maintaining homeostasis, which has garnered extensive attention from researchers worldwide. The holistic regulation bidirectional effects acupuncture can modulate autophagy, promoting or restoring homeostasis body's internal environment to achieve therapeutic outcomes. This paper systematically reviews research progress on use for treating various via autophagy pathway, summarizes signal pathways related analyzes deficiencies present existing research. review results indicate that mechanism action dysfunction is reflected changes LC3, Beclin1, p53, autophagy-associated (ATG) protein expression, regulates signaling key proteins genes. regulatory effect capacity bidirectional: it inhibits abnormal activation prevent exacerbation injury reduce apoptosis, while also activating enhancing promote elimination inflammation oxidative stress. Further analysis suggests are insufficiently explored. Future should prioritize development more appropriate animal models, analyzing accuracy relevant specificity indicators, exploring synergistic among targets pathways, clarifying at stages evaluating efficacy modulating. offers valuable insights into acupuncture.

Language: Английский

Emodin protects against severe acute pancreatitis-associated acute lung injury by activating Nrf2/HO-1/GPX4 signal and inhibiting ferroptosis in vivo and in vitro DOI Creative Commons
Gang Shen, Haiyun Wen, Huijuan Li

et al.

BMC Gastroenterology, Journal Year: 2025, Volume and Issue: 25(1)

Published: Feb. 5, 2025

Severe acute pancreatitis (SAP) has high morbidity, a complicated and dangerous course, many complications, including severe pulmonary complications. SAP-associated lung injury (SAP-ALI) is still significant challenge for surgeons because of its mortality. Therefore, more effective treatment methods are urgently needed. Emodin (EMO) shown tremendous potential in treating refractory diseases. However, protection mechanism SAP-ALI needs to be further clarified. This study was undertaken investigate the protective effects EMO against SAP rats alveolar epithelial cells, with particular focus on classical ferroptosis pathway. In an vivo study, forty SD were evenly split into five groups: sham operation (SO) group, biliopancreatic duct retrogradely injected 5% sodium taurocholate (STC) create + group administered via gavage following modeling, ML385 (a given inhibitor nuclear factor erythroid 2-related 2 (Nrf2)), group. vitro A549 cell lines exposed lipopolysaccharide (LPS) treated EMO. also used inhibit expression Nrf2. Pancreatic tissue damage evaluated using histological examination molecular experiments. Enzyme-linked immunosorbent assays (ELISA) assess levels pro-inflammatory cytokines, Fe2+, associated oxidative stress indicators serum supernatant. Real-time polymerase chain reaction (PCR), Western blot (WB), immunofluorescence find expressions related mRNAs proteins or cells. The findings demonstrated that suppressing Nrf2 exacerbated inflammatory response brought by pathological alterations SAP-ALI. reversed this change activating Nrf2/Heme Oxygenase-1 (HO-1)/glutathione peroxidase 4 (GPX4) signal path. Moreover, these results showed EMO, contrary ML385, suppressed response, which manifested as up-regulated glutathione (GSH) GPX4 down-regulated malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS) levels. Our effectively inhibited both vitro, while modulating Nrf2/HO-1/GPX4 signaling pathway provide

Language: Английский

Citations

1
Antimony-induced hippocampal neuronal impairment through ferroptosis activation from NCOA4-mediated ferritinophagy DOI

Shali Yu,

Zhiqiang Qin, Yuqing Chen

et al.

Chemico-Biological Interactions, Journal Year: 2025, Volume and Issue: unknown, P. 111415 - 111415

Published: Feb. 1, 2025

Language: Английский

Citations

1
Therapeutic Approaches with Iron Oxide Nanoparticles to Induce Ferroptosis and Overcome Radioresistance in Cancers DOI Creative Commons
Derek B. Sant’Angelo, Géraldine Descamps, Valentin Lecomte

et al.

Pharmaceuticals, Journal Year: 2025, Volume and Issue: 18(3), P. 325 - 325

Published: Feb. 26, 2025

The emergence of nanotechnology in medicine, particularly using iron oxide nanoparticles (IONPs), may impact cancer treatment strategies. IONPs exhibit unique properties, such as superparamagnetism, biocompatibility, and ease surface modification, making them ideal candidates for imaging, therapeutic interventions. Their application targeted drug delivery, especially with traditional chemotherapeutic agents like cisplatin, has shown potential overcoming limitations low bioavailability systemic toxicity chemotherapies. Moreover, IONPs, by releasing ions, can induce ferroptosis, a form iron-dependent cell death, which offers promising pathway to reverse radio- chemoresistance therapy. In particular, demonstrate significant radiosensitisers, enhancing the effects radiotherapy promoting reactive oxygen species (ROS) generation, lipid peroxidation, modulating tumour microenvironment stimulate antitumour immune responses. This review explores multifunctional roles radiosensitisation through ferroptosis induction, highlighting their promise advancing head neck cancers. Additional research is crucial fully addressing clinical settings, offering novel approach personalised treatment.

Language: Английский

Citations

1
TAX1BP1-dependent autophagic degradation of STING1 impairs anti-tumor immunity DOI
Ruoxi Zhang, Chunhua Yu,

Herbert J. Zeh

et al.

Autophagy, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 25, 2025

The activation of STING1 can lead to the production and secretion cytokines, initiating antitumor immunity. Here, we screened an ion channel ligand library identified tetrandrine, a bis-benzylisoquinoline alkaloid, as immunological adjuvant that enhances immunity by preventing autophagic degradation protein. This tetrandrine effect is independent its known function calcium or potassium blocker. Instead, inhibits lysosomal function, impairing cathepsin maturation, degradation. Proteomic analysis lysosomes TAX1BP1 novel receptor for proteolysis STING1. recognizes through physical interaction coiled-coil domain with cyclic dinucleotide binding Systematic mutation lysine (K) residues revealed K63-ubiquitination at K224 site ignites TAX1BP1-dependent Combined treatment agonists promotes converting "cold" pancreatic cancers into "hot" tumors. process associated enhanced cytokine release increased infiltration cytotoxic T-cells tumor microenvironment. mediated limited neutralizing antibodies type I interferon CD8+ T cells. Thus, these findings establish potential immunotherapeutic strategy against cancer

Language: Английский

Citations

1
SH3GL1‐activated FTH1 inhibits ferroptosis and confers doxorubicin resistance in diffuse large B‐cell lymphoma DOI Creative Commons

Zi‐Wen Duan,

Wei‐Ting Wang,

Yan Wang

et al.

Clinical and Translational Medicine, Journal Year: 2025, Volume and Issue: 15(3)

Published: March 1, 2025

Language: Английский

Citations

1
Compartmentalized mitochondrial ferroptosis converges with optineurin-mediated mitophagy to impact airway epithelial cell phenotypes and asthma outcomes DOI Creative Commons
Kazuhiro Yamada, Claudette M. St. Croix, Donna B. Stolz

et al.

Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)

Published: July 10, 2024

Abstract A stable mitochondrial pool is crucial for healthy cell function and survival. Altered redox biology can adversely affect mitochondria through induction of a variety death survival pathways, yet the understanding their dysfunction in primary human cells specific disease states, including asthma, modest. Ferroptosis traditionally considered an iron dependent, hydroperoxy-phospholipid executed process, which induces cytosolic damage to drive programmed death. However, this report we identify lipoxygenase orchestrated, compartmentally-targeted ferroptosis-associated peroxidation process occurs subpopulation dysfunctional mitochondria, without promoting Rather, tightly couples with PTEN-induced kinase (PINK)−1(PINK1)-Parkin-Optineurin mediated mitophagy effort preserve functional prevent These combined processes lead altered epithelial phenotypes loss ciliated associate worsened asthma severity. Ferroptosis-targeted interventions could reverse phenotypic changes improve outcomes.

Language: Английский

Citations

8
NFE2L2 and ferroptosis resistance in cancer therapy DOI Open Access
Daolin Tang, Rui Kang

Cancer Drug Resistance, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 25, 2024

NFE2-like basic leucine zipper transcription factor 2 (NFE2L2, also known as NRF2), is a key in the cellular defense against oxidative stress, playing crucial role cancer cell survival and resistance to therapies. This review outlines current knowledge on link between NFE2L2 ferroptosis - form of regulated death characterized by iron-dependent lipid peroxidation within cells. While activation can protect normal cells from damage, its overexpression contributes drug upregulating antioxidant defenses inhibiting ferroptosis. We delve into molecular pathways ferroptosis, highlighting involvement target genes, such

Language: Английский

Citations

8
Macroautophagy/autophagy promotes resistance to KRASG12D-targeted therapy through glutathione synthesis DOI Creative Commons
Leng Han,

Lingjun Meng,

Jiao Liu

et al.

Cancer Letters, Journal Year: 2024, Volume and Issue: 604, P. 217258 - 217258

Published: Sept. 13, 2024

Language: Английский

Citations

6
Mammalian nucleophagy: process and function DOI
Fujian Ji, Enyong Dai, Rui Kang

et al.

Autophagy, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 19, 2025

The nucleus is a highly specialized organelle that houses the cell's genetic material and regulates key cellular activities, including growth, metabolism, protein synthesis, cell division. Its structure function are tightly regulated by multiple mechanisms to ensure integrity genomic stability. Increasing evidence suggests nucleophagy, selective form of autophagy targets nuclear components, plays critical role in preserving clearing dysfunctional materials such as proteins (lamins, SIRT1, histones), DNA-protein crosslinks, micronuclei, chromatin fragments. Impaired nucleophagy has been implicated aging various pathological conditions, cancer, neurodegeneration, autoimmune disorders, neurological injury. In this review, we focus on mammalian cells, discussing its mechanisms, regulation, cargo selection, well evaluating therapeutic potential promoting human health mitigating disease.

Language: Английский

Citations

0
Molecular Insights in the Anticancer Activity of Natural Tocotrienols: Targeting Mitochondrial Metabolism and Cellular Redox Homeostasis DOI Creative Commons
Raffaella Chiaramonte,

Giulia Sauro,

Domenica Giannandrea

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 115 - 115

Published: Jan. 20, 2025

The role of mitochondria as the electric engine cells is well established. Over past two decades, accumulating evidence has pointed out that, despite presence a highly active glycolytic pathway (Warburg effect), functional and even upregulated mitochondrial respiration occurs in cancer to meet need high energy biosynthetic demand sustain their anabolic growth. Mitochondria are also primary source intracellular ROS. Cancer maintain moderate levels ROS promote tumorigenesis, metastasis, drug resistance; indeed, once cytotoxicity threshold exceeded, trigger oxidative damage, ultimately leading cell death. Based on this, metabolic functions generation considered attractive targets synthetic natural anticancer compounds. Tocotrienols (TTs), specifically δ- γ-TT isoforms, vitamin E-derived biomolecules widely shown possess striking properties since they regulate several molecular pathways. Herein, we provide for first time an overview reprogramming redox homeostasis perturbation occurring cells, highlighting involvement TTs. This sheds light use these compounds promising preventive or therapeutic approach novel strategies.

Language: Английский

Citations

0