Liver Fibrosis Leading to Cirrhosis: Basic Mechanisms and Clinical Perspectives DOI Creative Commons

Kaumudi Somnay,

Priyanka Wadgaonkar,

Nidhishri Sridhar

и другие.

Biomedicines, Год журнала: 2024, Номер 12(10), С. 2229 - 2229

Опубликована: Сен. 30, 2024

Liver fibrosis is the pathological deposition of extracellular matrix rich in fibrillar collagen within hepatocytes response to chronic liver injury due various causes. As condition advances, it can progress cirrhosis, late stages which are irreversible. Multiple pathophysiological mechanisms and cell types responsible for progression cirrhosis. Hepatic stellate cells myofibroblast activation represent a key event fibrosis. Capillarization sinusoidal endothelial further contributes an increase portal pressure. Macrophages neutrophils produce inflammatory cytokines participate activating hepatic cells. Although initially believed be irreversible, early now found reversible. Furthermore, advances noninvasive imaging serum studies have changed improved how cirrhosis evaluated monitored. there currently no specific approved therapies reverse fibrosis, management underlying diseases has been halt progression, extent, even preventing cirrhosis-related complications.

Язык: Английский

Immunosuppressive tumor microenvironment in the progression, metastasis, and therapy of hepatocellular carcinoma: from bench to bedside DOI Creative Commons
Yue Yin,

Weibo Feng,

Jie Chen

и другие.

Experimental Hematology and Oncology, Год журнала: 2024, Номер 13(1)

Опубликована: Авг. 1, 2024

Abstract Hepatocellular carcinoma (HCC) is a highly heterogeneous malignancy with high incidence, recurrence, and metastasis rates. The emergence of immunotherapy has improved the treatment advanced HCC, but problems such as drug resistance immune-related adverse events still exist in clinical practice. immunosuppressive tumor microenvironment (TME) HCC restricts efficacy essential for progression metastasis. Therefore, it necessary to elucidate mechanisms behind TME develop apply immunotherapy. This review systematically summarizes pathogenesis formation TME, by which accelerates We also status further discuss existing challenges potential therapeutic strategies targeting TME. hope inspire optimizing innovating immunotherapeutic comprehensively understanding structure function HCC.

Язык: Английский

Процитировано

19

A Guide to Pathophysiology, Signaling Pathways, and Preclinical Models of Liver Fibrosis DOI

Marjia Sultana,

Md Asrarul Islam,

Rhema Khairnar

и другие.

Molecular and Cellular Endocrinology, Год журнала: 2025, Номер unknown, С. 112448 - 112448

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

2

Emerging advanced approaches for diagnosis and inhibition of liver fibrogenesis DOI Creative Commons

Tamer A. Addissouky,

Majeed M. A. Ali, Ibrahim El Tantawy El Sayed

и другие.

The Egyptian Journal of Internal Medicine, Год журнала: 2024, Номер 36(1)

Опубликована: Фев. 12, 2024

Abstract Background Liver fibrosis results from chronic liver injury and is characterized by excessive deposition of extracellular matrix proteins including collagen. It can progress to cirrhosis failure. Main body the abstract Multiple cellular signaling pathways drive hepatic stellate cell activation fibrogenesis. Advances in biomarkers, imaging modalities, omics platforms enable noninvasive diagnosis staging fibrosis. Emerging antifibrotic approaches include medications like pirfenidone, obeticholic acid, monoclonal antibodies targeting pro-fibrotic mediators. Cell therapies using mesenchymal stem cells demonstrate potential through paracrine immunosuppression. Tissue-engineered grafts biomaterial carriers for localized drug delivery are promising technologies. Microfluidic liver-on-a-chip with patient-derived provide unprecedented models study human test candidates. Short conclusion Significant has elucidated mechanisms underlying fibrogenesis uncovered novel therapeutic targets. Ongoing challenges translating preclinical findings, improving efficacy, enabling personalized precision medicine approaches. Further research into combinatorial therapies, tissue engineering technologies will advance treatment all causes.

Язык: Английский

Процитировано

9

The evidence-based multifaceted roles of hepatic stellate cells in liver diseases: A concise review DOI
Jong‐Won Kim,

Yu Ji Kim

Life Sciences, Год журнала: 2024, Номер 344, С. 122547 - 122547

Опубликована: Март 7, 2024

Язык: Английский

Процитировано

8

Recent advances in polymeric nanoparticles for the treatment of hepatic diseases DOI Creative Commons
Feng Gao,

Xuefei Feng,

Xinyu Li

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Янв. 24, 2025

The liver performs crucial roles in energy metabolism, detoxification, and immune regulation. Hepatic diseases, including hepatitis, fibrosis, cancer, have posed a significant threat to global health, emphasizing the critical need for development of novel effective treatment approaches. Nanotechnology, an emerging technology, has been extensively researched medicine. Among many types nanomaterials, polymeric nanoparticles (NPs) are widely used drug delivery systems. Compared traditional therapies, they offer advantages disease by improving outcomes reducing side effects. This review introduced discussed application natural polymers synthetic their management. Furthermore, this paper reviewed -mainly chitosan (CS), hyaluronic acid (HA), polyethylene glycol (PEG) poly (lactic-co-glycolic acid) (PLGA)-in treatment, focusing on use various systems pure bioactive compounds origin, drugs, nucleic acids, peptides, others. Finally, challenges future perspectives NPs were provide guidance further research directions, with aim promoting clinical nanotherapeutics treating hepatic diseases.

Язык: Английский

Процитировано

1

Preclinical Promise and Clinical Challenges for Innovative Therapies Targeting Liver Fibrogenesis DOI Creative Commons

Tamer A. Addissouky,

Majeed M. A. Ali, Ibrahim El Tantawy El Sayed

и другие.

Archives of Gastroenterology Research, Год журнала: 2023, Номер 4(1), С. 14 - 23

Опубликована: Ноя. 14, 2023

Liver fibrosis resulting from chronic liver injury can progress to cirrhosis and failure. Current treatments are limited, creating an urgent need for novel antifibrotic therapies. Multiple emerging approaches have shown preclinical promise in inhibiting fibrogenesis or stimulating regeneration, including artificial support, stem cell therapy, cell/gene nanomedicines, immunotherapy, herbal medicines. Artificial support provides detoxification but has inconsistent transplant bridging benefits. Stem transplantation demonstrates paracrine effects differentiation potential. Cell therapy with hepatocytes modulatory immune cells, as well genetic engineering approaches, aims replace damaged cells suppress inflammation. Nanoparticles enable targeted delivery of drugs genes. Immunotherapy using checkpoint inhibitors, vaccines, engineered attenuate fibrogenesis-related Some traditional Chinese formulas compounds exhibit antifibrotic, anti-inflammatory, regenerative mechanisms. Despite encouraging data, most therapies yet achieve clinical translation, limited by challenges safety, delivery, efficacy. Combination treatment regimens may provide maximal therapeutic impact. Ongoing optimization rigorous evaluation needed develop effective new patients disease.

Язык: Английский

Процитировано

21

Kidney Fibrosis: Fundamental Questions, Challenges, and Perspectives DOI
Youhua Liu

Integrative Medicine in Nephrology and Andrology, Год журнала: 2024, Номер 11(4)

Опубликована: Окт. 1, 2024

Язык: Английский

Процитировано

6

Structural characterization of an inulin neoseries-type fructan from Ophiopogonis Radix and the therapeutic effect on liver fibrosis in vivo DOI
Wei Liu,

Linzhang Zhang,

Wei Xia

и другие.

Carbohydrate Polymers, Год журнала: 2023, Номер 327, С. 121659 - 121659

Опубликована: Дек. 4, 2023

Язык: Английский

Процитировано

13

Ferroptosis in Liver Disease: Natural Active Compounds and Therapeutic Implications DOI Creative Commons

Zhili Wu,

Yanru Zhu,

Wen‐Chao Liu

и другие.

Antioxidants, Год журнала: 2024, Номер 13(3), С. 352 - 352

Опубликована: Март 15, 2024

Ferroptosis is an emerging type of regulated cell death usually accompanied by the accumulation ferrous ions (Fe2+) and lipid peroxides. As metabolic hub body, liver crucial for iron storage metabolism. The seems to be closely related ferroptosis through Liver disease greatly threatens host health, exploring effective interventions essential. Mounting studies have demonstrated that one possible pathogenic mechanisms involved in disease. Targeting may provide a promising opportunity treating However, drugs targeting are extremely limited. Therefore, it urgent need develop new safe regulators. Natural active compounds (NAC), especially those derived from traditional Chinese medicine, recently shown great therapeutic potential via modulating ferroptosis-related genes or pathways. Here, we outline molecular mechanism systematically summarize regulatory function NAC on Finally, discuss application prospects problems concerning as regulators managing

Язык: Английский

Процитировано

5

Ginsenoside Rb1 induces hepatic stellate cell ferroptosis to alleviate liver fibrosis via the BECN1/SLC7A11 axis DOI Creative Commons

Lifan Lin,

Xinmiao Li, Yifei Li

и другие.

Journal of Pharmaceutical Analysis, Год журнала: 2023, Номер 14(5), С. 100902 - 100902

Опубликована: Ноя. 29, 2023

Liver fibrosis is primarily driven by the activation of hepatic stellate cells (HSCs), a process associated with ferroptosis. Ginsenoside Rb1 (GRb1), major active component extracted from Panax ginseng, inhibits HSC activation. However, potential role GRb1 in mediating ferroptosis remains unclear. This study examined effect on liver both vivo and vitro, using CCl4-induced mouse model primary HSCs, LX-2 cells. The findings revealed that effectively inactivated HSCs reducing alpha-smooth muscle actin Type I collagen levels. Moreover, significantly alleviated vivo. From mechanistic standpoint, pathway appeared to be central antifibrotic effects GRb1. Specifically, promoted characterized increased glutathione depletion, malondialdehyde production, iron overload, accumulation reactive oxygen species. Intriguingly, Beclin 1 (BECN1) levels decreased System Xc-key subunit SLC7A11. Further experiments showed BECN1 silencing inhibited GRb1-induced mitigated reduction SLC7A11 caused could directly interact SLC7A11, initiating In conclusion, suppression counteracted inactivation vitro. Overall, this highlights novel inducing promoting inactivation, at least partly through its modulation

Язык: Английский

Процитировано

12