Advances in Research on the Effectiveness and Mechanism of Active Ingredients from Traditional Chinese Medicine in Regulating Hepatic Stellate Cells Autophagy Against Hepatic Fibrosis DOI Creative Commons
Xin Yu Liu, Wei Zhang,

Bao-Feng Ma

et al.

Drug Design Development and Therapy, Journal Year: 2024, Volume and Issue: Volume 18, P. 2715 - 2727

Published: July 1, 2024

Abstract: Hepatic fibrosis (HF) is a pathological process of structural and functional impairment the liver key component in progression chronic disease. There are no specific anti-hepatic (anti-HF) drugs, HF can only be improved or prevented by alleviating cause. Autophagy hepatic stellate cells (HSCs) closely related to development HF. In recent years, traditional Chinese medicine (TCM) has achieved good therapeutic effects prevention treatment Several active ingredients from TCM (AITCM) regulate autophagy HSCs exert anti-HF through different pathways, but relevant reviews lacking. This paper reviewed research progress AITCM regulating against HF, also discussed relationship between pointing out problems limitations current study, order provide references for drugs targeting TCM. By reviewing literature PubMed, Web Science, Embase, CNKI other databases, we found that currently controversial. may promote consuming lipid droplets (LDs) energy their activation. However, contrast, inducing effect stimulating apoptosis senescence, reducing type I collagen accumulation, inhibiting extracellular vesicles release, degrading pro-fibrotic factors mechanisms. Some inhibit resist with most promising direction being target LDs. While, others induce apoptosis. Future needs focus on cell research, vivo verification explore reasons contradictory Keywords: fibrosis, autophagy, medicine, activation

Language: Английский

The role of PI3k/AKT signaling pathway in attenuating liver fibrosis: a comprehensive review DOI Creative Commons
Emad Shamsan,

Maged Almezgagi,

Mohammed Gamah

et al.

Frontiers in Medicine, Journal Year: 2024, Volume and Issue: 11

Published: March 25, 2024

Excessive accumulation of extracellular matrix (ECM) components within the liver leads to a pathological condition known as fibrosis. Alcohol abuse, non-alcoholic fatty disease (NAFLD), autoimmune issues, and viral hepatitis cause chronic injury. Exploring potential therapeutic targets understanding molecular mechanisms involved in fibrosis are essential for development effective interventions. The goal this comprehensive review is explain how PI3K/AKT signaling pathway contributes reduction target investigated through summary results from vivo vitro studies. Studies focusing on activation have shown significant decrease markers improvement function. emphasizes may prevent ECM synthesis hepatic stellate cell (HSC) activation, ultimately reducing fibrotic response. specific downstream effectors constitute rapidly developing field study. In conclusion, plays role attenuating Its complex regulating HSC production, demonstrated both , underscores its approach managing slowing progression. A provides valuable insights into future developments implications clinical applications.

Language: Английский

Citations

23
Cigarette Smoke Contributes to the Progression of MASLD: From the Molecular Mechanisms to Therapy DOI Creative Commons
Jihao Xu, Yifan Li,

Zhaolan Feng

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(3), P. 221 - 221

Published: Feb. 4, 2025

Cigarette smoke (CS), an intricate blend comprising over 4000 compounds, induces abnormal cellular reactions that harm multiple tissues. Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic (CLD), encompassing non-alcoholic (NAFL), steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). Recently, the term NAFLD has been changed to metabolic dysfunction-associated steatotic (MASLD), NASH renamed (MASH). A multitude of experiments have confirmed association between CS incidence progression MASLD. However, specific signaling pathways involved need be updated with new scientific discoveries. exposure can disrupt lipid metabolism, induce inflammation apoptosis, stimulate fibrosis through promote Currently, there no officially approved efficacious pharmaceutical intervention in clinical practice. Therefore, lifestyle modifications emerged as primary therapeutic approach for managing Smoking cessation application series natural ingredients shown ameliorate pathological changes induced by CS, potentially serving effective decelerating MASLD development. This article aims elucidate which smoking promotes MASLD, while summarizing reversal factors identified recent studies, thereby offering novel insights future research on treatment

Language: Английский

Citations

2
Therapeutic targeting of TGF‐β in lung cancer DOI Creative Commons

Sajjad Aftabi,

Amir Barzegar Behrooz, Marco Cordani

et al.

FEBS Journal, Journal Year: 2024, Volume and Issue: unknown

Published: July 31, 2024

Transforming growth factor‐β (TGF‐β) plays a complex role in lung cancer pathophysiology, initially acting as tumor suppressor by inhibiting early‐stage growth. However, its evolves the advanced stages of disease, where it contributes to progression not directly promoting cell proliferation but enhancing epithelial–mesenchymal transition (EMT) and creating conducive microenvironment. While EMT is typically associated with enhanced migratory invasive capabilities rather than per se , TGF‐β's influence on this process facilitates dynamics metastasis. Additionally, TGF‐β impacts microenvironment interacting immune cells, influenced genetic epigenetic changes within cells. This interaction highlights evasion chemoresistance, further complicating therapy. review provides critical overview recent findings involvement cancer, contribution modulation response. Despite considerable challenges encountered clinical trials development new treatments targeting pathway, necessity for continued, in‐depth investigation into roles TGF‐β. A deeper comprehension these may lead novel, targeted therapies cancer. intricate behavior signaling tumors previous challenges, research could yield innovative treatment strategies.

Language: Английский

Citations

7
The SGLT2 inhibitor empagliflozin inhibits skeletal muscle fibrosis in naturally aging male mice through the AMPKα/MMP9/TGF-β1/Smad pathway DOI
Qixuan Huang, Jie Chen,

Siqi Liao

et al.

Biogerontology, Journal Year: 2024, Volume and Issue: 25(3), P. 567 - 581

Published: Feb. 26, 2024

Language: Английский

Citations

6
Nuciferine Restores Autophagy via the PI3K-AKT-mTOR Pathway to Alleviate Renal Fibrosis in Diabetic Kidney Disease DOI

Tongqing Li,

Huijian Chen,

Yan Guo

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: 73(9), P. 5223 - 5235

Published: Feb. 24, 2025

Diabetic kidney disease (DKD) is one of the complications diabetes mellitus, which triggers fibrosis and eventually develops into end-stage renal disease. Nuciferine (NF) most important functional components in lotus leaves (LL), but its role mechanism for treatment DKD are unclear. A high-fat-diet (HFD)-induced model KK-AY mice was established this study. NF significantly improved blood glucose biochemical indices mice. Furthermore, reduced levels mALB, UCRE, Scr, BUN urine. Further, extent lesions study at stage IV according to Mogensen staging method. effective ameliorating injury during period. Concurrently, protein FN, N-cadherin, TGFβ, p-Smad3, p-PI3K, p-AKT, p-mTOR, p62 were decreased. In contrast, level expression Beclin-1 increased. high glucose-exposed HK-2 cell model, p-mTOR all downregulated, autophagy proteins increased after intervention. addition, cells treated with combination Wortmannin 3-MA, respectively. The results demonstrated that inhibited TGFβ p-Smad3 by regulating through PI3K-AKT-mTOR pathway, thereby Therefore, LL can be used as a dietary component prevention patients.

Language: Английский

Citations

0
Nets in fibrosis: Bridging innate immunity and tissue remodeling DOI
Xueni Ma,

LI Ji-pin,

Muyang Li

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 137, P. 112516 - 112516

Published: June 20, 2024

Language: Английский

Citations

3
Recent advances of nanomaterials in imaging liver fibrosis DOI Creative Commons
Jin Cui, Shuxuan Zhang,

Xueli Xu

et al.

BMEMat, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 16, 2024

Abstract Liver fibrosis is a pathological process resulting from prolonged exposure to various injury factors. It characterized by the abnormal proliferation and activation of hepatic stellate cells excessive deposition extracellular matrix. If left untreated, it can progress cirrhosis, liver failure, even cancer. There currently no efficient accurate clinical diagnostic method for early fibrosis. Therefore, there an urgent need address challenge staging diagnosis in practice. Recently, nanomaterials have demonstrated significant potential enhancing Nanomaterials possess ability precisely identify target microenvironment associated with By their enrichment area, improve imaging contrast lesions liver, thereby enabling Accordingly, this review delves into latest research advancements concerning diagnosis.

Language: Английский

Citations

3
Recent advances in therapeutic use of transforming growth factor-beta inhibitors in cancer and fibrosis DOI Creative Commons
Jing He, Yan Gao, Linyuan Jing

et al.

Frontiers in Oncology, Journal Year: 2025, Volume and Issue: 15

Published: April 25, 2025

Transforming growth factor-beta (TGF-β) has long been known to be associated with early embryonic development and organogenesis, immune supervision, tissue repair homeostasis in adults. TGF-β complex roles fibrosis cancer that may opposing at different stages of these diseases. Under pathological conditions, overexpression causes epithelial-mesenchymal transition, deposition extracellular matrix, formation cancer-associated fibroblasts, leading fibrotic disease or cancer. Fibroblasts, epithelial cells, cells are the most common targets TGF-β, while TGF-β-associated Given critical role its downstream molecules progression cancer, therapies targeting signaling appear a promising strategy. Preclinical clinical studies have investigated including antisense oligonucleotides, monoclonal antibodies, ligand traps. However, targeted therapy hindered by systemic cytotoxicity. This review discusses molecular mechanisms highlights for as therapeutic strategy related

Language: Английский

Citations

0
Autophagy and Biomaterials: A Brief Overview of the Impact of Autophagy in Biomaterial Applications DOI Creative Commons
Leila Pirmoradi, Shahla Shojaei, Saeid Ghavami

et al.

Pharmaceutics, Journal Year: 2023, Volume and Issue: 15(9), P. 2284 - 2284

Published: Sept. 5, 2023

Macroautophagy (hereafter autophagy), a tightly regulated physiological process that obliterates dysfunctional and damaged organelles proteins, has crucial role when biomaterials are applied for various purposes, including diagnosis, treatment, tissue engineering, targeted drug delivery. The unparalleled physiochemical properties of nanomaterials make them key component medical strategies in different areas, such as osteogenesis, angiogenesis, neurodegenerative disease cancer therapy. application implants their modulatory effects on autophagy have been known recent years. However, more studies necessary to clarify the interactions all involved mechanisms. advantages disadvantages nanomaterial-mediated need serious attention both biological bioengineering fields. In this mini-review, after biomaterial exploitation possible related mechanisms explored.

Language: Английский

Citations

6
Stromal interaction molecule 1/microtubule‐associated protein 1A/1B‐light chain 3B complex induces metastasis of hepatocellular carcinoma by promoting autophagy DOI Creative Commons

Jingchun Wang,

Qichao Xie, Lei Wu

et al.

MedComm, Journal Year: 2024, Volume and Issue: 5(2)

Published: Feb. 1, 2024

Metastasis is the leading cause of death in hepatocellular carcinoma (HCC) patients, and autophagy plays a crucial role this process by orchestrating epithelial-mesenchymal transition (EMT). Stromal interaction molecule 1 (STIM1), central regulator store-operated calcium entry (SOCE) nonexcitable cells, involved development spread HCC. However, impact STIM1 on regulation during HCC metastasis remains unclear. Here, we demonstrate that temporally regulated autophagy-induced EMT knocking out (KO) significantly reduces both EMT. Interestingly, enhances through SOCE-dependent independent pathways. Mechanistically, directly interacts with microtubule-associated protein 1A/1B-light chain 3B (LC3B) to form complex via sterile-α motif (SAM) domain, which promotes autophagosome formation. Furthermore, deletion SAM domain abolishes its binding LC3B, decrease cells. These findings unveil novel mechanism STIM1/LC3B mediates highlighting potential target for preventing metastasis.

Language: Английский

Citations

2