Autophagy in aging-related diseases and cancer: Principles, regulatory mechanisms and therapeutic potential

Ageing Research Reviews, Год журнала: 2024, Номер 100, С. 102428 - 102428

Опубликована: Июль 20, 2024

Язык: Английский

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Role of mitochondria in pathogenesis and therapy of renal fibrosis

Metabolism, Год журнала: 2024, Номер 155, С. 155913 - 155913

Опубликована: Апрель 11, 2024

Язык: Английский

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Lycopene from tomatoes and tomato products exerts renoprotective effects by ameliorating oxidative stress, apoptosis, pyroptosis, fibrosis, and inflammatory injury in calcium oxalate nephrolithiasis: the underlying mechanisms

Food & Function, Год журнала: 2024, Номер 15(8), С. 4021 - 4036

Опубликована: Янв. 1, 2024

Several mechanisms underlying nephrolithiasis, one of the most common urological diseases, involve calcium oxalate formation, including oxidative stress, inflammatory reactions, fibrosis, pyroptosis, and apoptosis.

Язык: Английский

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Identification of biomarkers for chronic renal fibrosis and their relationship with immune infiltration and cell death

Renal Failure, Год журнала: 2025, Номер 47(1)

Опубликована: Янв. 8, 2025

Background Chronic kidney disease (CKD) represents a significant global public health challenge. This study aims to identify biomarkers of renal fibrosis and elucidate the relationship between unilateral ureteral obstruction (UUO), immune infiltration, cell death.

Язык: Английский

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Bisphenol A induces apoptosis and disrupts testosterone synthesis in TM3 cells via reactive oxygen species-mediated mitochondrial pathway and autophagic flux inhibition

Ecotoxicology and Environmental Safety, Год журнала: 2025, Номер 289, С. 117691 - 117691

Опубликована: Янв. 1, 2025

Bisphenol A (BPA) is a common endocrine disruptor chemical that widely used in the production of food plastic packaging, and it has been shown to potentially harm reproductive system. However, specific mechanism by which BPA induces apoptosis Leydig cells (LCs) inhibits testosterone synthesis these unclear. In present study, TM3 were as an experimental model combination with reactive oxygen species (ROS) scavenger (N-acetylcysteine), Caspase-3 inhibitor (Ac-DEVD-CHO), autophagy activator (Torin2), (Chloroquine) investigate potential mechanisms causes cell damage vitro. treatment increased ROS production, led marked decrease antioxidant enzyme activity expression levels antioxidant-related genes proteins cells. Upregulated cause excessive opening mitochondrial permeability transition pore significantly related membrane function The release cytochrome C from damaged mitochondria into cytoplasm activated Caspase cascade reaction. addition, impaired autophagic degradation inhibiting fusion autophagosomes lysosomes. These abnormalities eventually induced inhibited collective findings suggest interferes upregulating thereby activating apoptotic pathway flux. provide novel mechanistic insights male toxicity caused exposure.

Язык: Английский

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Danshen injection ameliorates unilateral ureteral obstruction-induced renal fibrosis by inhibiting ferroptosis via activating SIRT1/GPX4 pathway

Frontiers in Pharmacology, Год журнала: 2025, Номер 15

Опубликована: Янв. 13, 2025

The pathogenesis of renal fibrosis is related to blood stasis, and the method promoting circulation removing stasis often used as treatment principle. Danshen injection (DSI) a commonly drug for in clinic. However, whether DSI slows progression or potential mechanism uncertain. We investigated models using UUO mice TGF-β stimulation HK-2 cells. Our findings revealed that Fer-1 alleviated kidney injury by ameliorating morphology pathological vivo. Besides, inhibited vivo TGF-β-induced Furthermore, ferroptosis was lessened under treatment. More importantly, active ingredients (danshensu, salvianolic acid B, protocatechuic aldehyde, caffeic tanshinone IIA) could bind SIRT1. protein levels SIRT1 GPX4 were downregulated accompanied incremental concentrations Erastin, which repaired intervention. inhibition owing reversed inhibitor EX527. Taken together, our results indicated protect against attenuate activating SIRT1/GPX4 pathway. It expected be agent treat fibrosis.

Язык: Английский

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Non-lethal sonodynamic therapy mitigates hypertensive renal fibrosis through the PI3K/AKT/mTORC1-autophagy pathway

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Фев. 6, 2025

Hypertension constitutes a significant public health concern, characterized by high incidence and mortality rate. Hypertensive kidney disease is prevalent complication associated with hypertension the second leading cause of end-stage renal (ESRD). Renal fibrosis linked to has emerged as third in dialysis patients. Autophagy activity crucial for maintaining homeostasis, vitality, physiological function cells, while also protecting kidneys from fibrosis. The deficiency autophagy will increase sensitivity damage, impaired function, accumulation damaged mitochondria more severe However, enhancing activating PI3K/AKT, AMPK, mTOR pathways, improves podocyte injury pathological changes, ameliorates function. Current clinical interventions aimed at halting or reversing hypertensive patients are notably limited their efficacy. Here, we present Non-lethal Sonodynamic Therapy (NL-SDT), which ultrasound used activate locally sonosensitizers, thereby stimulating production reactive oxygen species purpose modulating cell fate, novel methodology inhibit progression To confirm whether NL-SDT can reduce its mechanism. mice model was established using osmotic minipumps (Alzet 2004, Cupertino, CA) equipped angiotensin-II (Ang II). pumps were implanted mice, ensuring constant infusion Ang II dose 1.0 µg/kg per minute 4 weeks. exposed 0.4 W/cm2 intensity ultrasonic radiation 15 min h post injection sinoporphyrin sodium (DVDMS) (4 mg/kg) into caudal vein repeated weekly treatments. stained masson's trichrome staining collagen fiber expression, alpha-smooth muscle actin (α-SMA) expression determined via immunohistochemical staining. protein levels parameters (α-SMA, I, vimentin), pathway-related proteins (PI3K, AKT, mTORC1) autophagy-related LC3B western blotting. Intracellular (ROS) detected DCFH-DA probe. Immunofluorescence observe α-SMA E-cadherin cells. Pathway-related inhibitors (the inhibitor 3-methyladenine (3-MA), chloroquine (CQ), ROS N-acetyl-L-cysteine (NAC) applied, autophagosome changes observed under transmission electron microscopy. LC3 spot formation within We obtained following results animal cellular research. In vivo, (1) area tissue increased significantly group (50.6%). positive (37.8%). (2) decreased after treatment (34.8%). too (48.9%). group. (3) effect on reducing be changed rapamycin CQ. vitro. α-SMA, I vimentin TGF-β1-induced NRK-52E autophagosomes cells NL-SDT. (24.8%). reversed administration NAC. PI3K, P-AKT P-mTORC1 inhibited transition epithelial myofibroblasts PI3K-AKT-mTORC1-autophagy pathway showed reciprocal NL-SDT-inhibited epithelial-mesenchymal (EMT). reduced blood pressure temporarily induced II. alleviated promoted inhibiting PI3K-AKT-mTORC1 signaling non-invasive efficacious regimen It may new approach fibrosis, delaying occurrence ESRD.

Язык: Английский

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Targeting proteostasis network in osteoporosis: Pathological mechanisms and therapeutic implications

Ageing Research Reviews, Год журнала: 2023, Номер 90, С. 102024 - 102024

Опубликована: Июль 31, 2023

As the most common bone disease, osteoporosis (OP) increases fragility and makes patients more vulnerable to threat of osteoporotic fractures. With ageing population in today's society, OP has become a huge growing public health problem. Unfortunately, clear pathogenesis is still under exploration, effective interventions are scarce. Therefore, exploring new targets for pharmacological develop promising therapeutic drugs great clinical value. Previous studies have shown that normal remodeling depends on proteostasis, whereas loss proteostasis during leads dysfunctional network (PN) fails maintain homeostasis. Nevertheless, only few revealed pathophysiological relationship between metabolism single component PN, yet role PN as whole investigation. This review comprehensively summarized further discussed potential innovative drug therapy OP.

Язык: Английский

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Targeted degradation of NDUFS1 by agrimol B promotes mitochondrial ROS accumulation and cytotoxic autophagy arrest in hepatocellular carcinoma

Free Radical Biology and Medicine, Год журнала: 2024, Номер 220, С. 111 - 124

Опубликована: Апрель 30, 2024

Язык: Английский

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Adipose stem cell exosomes promote mitochondrial autophagy through the PI3K/AKT/mTOR pathway to alleviate keloids

Stem Cell Research & Therapy, Год журнала: 2024, Номер 15(1)

Опубликована: Сен. 15, 2024

Язык: Английский

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