نتائج البحث - "liver regeneration"

1

Dysregulation of miR-21-associated miRNA regulatory networks by chronic ethanol consumption impairs liver regeneration

المؤلفون: Rajanikanth Vadigepalli, Egle Juskeviciute, Jan B. Hoek, Austin Parrish, Ankita Srivastava

المصدر: Physiological Genomics. 53:546-555

الوصف: Impaired liver regeneration has been considered as a hallmark of progression of alcohol-associated liver disease. Our previous studies demonstrated that in vivo inhibition of the microRNA (miRNA) miR21 can restore regenerative capacity of the liver in chronic ethanol-fed animals. The present study focuses on the role of microRNA regulatory networks that are likely to mediate the miR-21 action. Rats were chronically fed an ethanol-enriched diet along with pair-fed control animals and treated with AM21 (anti-miR-21), a locked nucleic acid antisense to miR-21. Partial hepatectomy (PHx) was performed and miRNA expression profiling over the course of liver regeneration was assessed. Our results showed dynamic expression changes in several miRNAs after PHx, notably with altered miRNA expression profiles between ethanol and control groups. We found that in vivo inhibition of miR-21 led to correlated differential expression of miR-340-5p and anticorrelated expression of miR-365, let-7a, miR-1224, and miR-146a across all sample groups after PHx. Gene set enrichment analysis identified a miRNA signature significantly associated with hepatic stellate cell activation within whole liver tissue data. We hypothesized that at least part of the PHx-induced miRNA network changes responsive to miR-21 inhibition is localized to hepatic stellate cells. We validated this hypothesis using AM21 and TGF-β treatments in LX-2 human hepatic stellate cells in culture and measured expression levels of select miRNAs by quantitative RT-PCR. Based on the in vivo and in vitro results, we propose a hepatic stellate cell miRNA regulatory network as contributing to the restoration of liver regenerative capacity by miR-21 inhibition.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b373ea7fe25c44299bde8db462aab8cf
https://doi.org/10.1152/physiolgenomics.00113.2021

2

CoQ10 Promotes Resolution of Necrosis and Liver Regeneration After Acetaminophen-Induced Liver Injury

المؤلفون: Xu Chen, Peiwen Zhang, Taiping He, Yi Tang, Wanjun Fang, Shen Chen

المصدر: Toxicological Sciences. 185:19-27

الوصف: Coenzyme Q10 (CoQ10) which acts as an electron transporter in the mitochondrial respiratory chain has many beneficial effects on liver diseases. In our previous research, CoQ10 has been found to attenuate acetaminophen (APAP)-induced acute liver injury (ALI). However, whether CoQ10 administration is still effective at the late stage of APAP overdose is still unknown. In this study, we aimed to test CoQ10 efficacy at the late stage of APAP overdose. C57BL/6J mice were intraperitoneally treated with APAP to induce liver injury. CoQ10 (5 mg/kg) was given to mice at 16 h after APAP treatment. The results showed that while CoQ10 treatment at 16 h post-APAP overdose had no effects on the expression of ROS generated genes or scavenged genes, it still significantly decreased necrosis of hepatocytes following APAP-induced ALI. Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis. CoQ10 treatment also significantly enhanced hepatocytes proliferation as shown in the increased 5-bromodeoxyuridine incorporation in the APAP-intoxicated mice liver section. In addition, CoQ10 treatment increased hepatic Proliferating Cell Nuclear Antigen (PCNA) and Cyclin D1 expression and promoted activation of the β-catenin signaling in APAP-overdose mice. To conclude, these data provide evidence that CoQ10 treatment is still effective at the late stage of APAP-induced ALI and promotes resolution of necrosis and liver regeneration following ALI.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ac5f145915f43031bffeebb9861eedf5
https://doi.org/10.1093/toxsci/kfab123

3

Hepatic NF‐κB‐Inducing Kinase and Inhibitor of NF‐κB Kinase Subunit α Promote Liver Oxidative Stress, Ferroptosis, and Liver Injury

المؤلفون: Yi Xiong, Xiao Zhong, Yong Liu, Yatrik M. Shah, Hong Shen, Zhiguo Zhang, Xue-Gong Fan, Liangyou Rui

المصدر: Hepatology Communications, Vol 5, Iss 10, Pp 1704-1720 (2021)
Hepatology Communications

الوصف: Drug‐induced hepatotoxicity limits development of new effective medications. Drugs and numerous endogenous/exogenous agents are metabolized/detoxified by hepatocytes, during which reactive oxygen species (ROS) are generated as a by‐product. ROS has broad adverse effects on liver function and integrity, including damaging hepatocyte proteins, lipids, and DNA and promoting liver inflammation and fibrosis. ROS in concert with iron overload drives ferroptosis. Hepatic nuclear factor kappa B (NF‐κB)‐inducing kinase (NIK) is aberrantly activated in a broad spectrum of liver disease. NIK phosphorylates and activates inhibitor of NF‐κB kinase subunit alpha (IKKα), and the hepatic NIK/IKKα cascade suppresses liver regeneration. However, the NIK/IKKα pathway has not been explored in drug‐induced liver injury. Here, we identify hepatic NIK as a previously unrecognized mediator for acetaminophen (APAP)‐induced acute liver failure. APAP treatment increased both NIK transcription and NIK protein stability in primary hepatocytes as well as in liver in mice. Hepatocyte‐specific overexpression of NIK augmented APAP‐induced liver oxidative stress in mice and increased hepatocyte death and mortality in a ROS‐dependent manner. Conversely, hepatocyte‐specific ablation of NIK or IKKα mitigated APAP‐elicited hepatotoxicity and mortality. NIK increased lipid peroxidation and cell death in APAP‐stimulated primary hepatocytes. Pretreatment with antioxidants or ferroptosis inhibitors blocked NIK/APAP‐induced hepatocyte death. Conclusion: We unravel a previously unrecognized NIK/IKKα/ROS/ferroptosis axis engaged in liver disease progression.
Hepatic NIK is upregulated in response to hepatic toxicants. Ablation of hepatic NIK attenuates, whereas hepatocyte‐specific overexpression of NIK aggravates, APAP‐induced liver injury. NIK promotes hepatic oxidative stress and ferroptosis.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::396ba55de0694c8872057595c8698943
https://doi.org/10.1002/hep4.1757

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4

Depletion of essential isoprenoids and ER stress induction following acute liver-specific deletion of HMG-CoA reductase

المؤلفون: Mia Furgurson, Ayrea Hurley, Jun Han, Alexandria M. Doerfler, Ang Li, Jason C. Burton, Christoph H. Borchers, Marco De Giorgi, William R. Lagor, Rachel H. Hsu, Kalyani R. Patel, Kelsey E Jarrett

المصدر: J Lipid Res
Journal of Lipid Research, Vol 61, Iss 12, Pp 1675-1686 (2020)

مصطلحات موضوعية: 0301 basic medicine, adeno-associated virus, QD415-436, 030204 cardiovascular system & hematology, Reductase, Biochemistry, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Endocrinology, Dolichol, Genetic model, cholesterol synthesis and regulation, Research Articles, Cell metabolism, biology, Terpenes, Cell Biology, 3-hydroxy-3-methylglutaryl-coenzyme A, Endoplasmic Reticulum Stress, animal models, Liver regeneration, Cell biology, Dehydrodolichyl diphosphate synthase, endoplasmic reticulum, 030104 developmental biology, chemistry, Liver, HMG-CoA reductase, biology.protein, Unfolded protein response, lipids (amino acids, peptides, and proteins), Hydroxymethylglutaryl CoA Reductases, Mevalonate pathway, Gene Deletion

الوصف: HMG-CoA reductase (Hmgcr) is the rate-limiting enzyme in the mevalonate pathway and is inhibited by statins. In addition to cholesterol, Hmgcr activity is also required for synthesizing nonsterol isoprenoids, such as dolichol, ubiquinone, and farnesylated and geranylgeranylated proteins. Here, we investigated the effects of Hmgcr inhibition on nonsterol isoprenoids in the liver. We have generated new genetic models to acutely delete genes in the mevalonate pathway in the liver using AAV-mediated delivery of Cre-recombinase (AAV-Cre) or CRISPR/Cas9 (AAV-CRISPR). The genetic deletion of Hmgcr by AAV-Cre resulted in extensive hepatocyte apoptosis and compensatory liver regeneration. At the biochemical level, we observed decreased levels of sterols and depletion of the nonsterol isoprenoids, dolichol and ubiquinone. At the cellular level, Hmgcr-null hepatocytes showed ER stress and impaired N-glycosylation. We further hypothesized that the depletion of dolichol, essential for N-glycosylation, could be responsible for ER stress. Using AAV-CRISPR, we somatically disrupted dehydrodolichyl diphosphate synthase subunit (Dhdds), encoding a branch point enzyme required for dolichol biosynthesis. Dhdds-null livers showed ER stress and impaired N-glycosylation, along with apoptosis and regeneration. Finally, the combined deletion of Hmgcr and Dhdds synergistically exacerbated hepatocyte ER stress. Our data show a critical role for mevalonate-derived dolichol in the liver and suggest that dolichol depletion is at least partially responsible for ER stress and apoptosis upon potent Hmgcr inhibition.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::770616831edb479aac432495d2555db3

5

Pterostilbene alleviates liver ischemia/reperfusion injury via PINK1-mediated mitophagy

المؤلفون: Chuanlong Guo, Guangfen Zhao, Susu Wei, Qiangqiang Shi, Xianggen Wu, Robert Chunhua Zhao, Guohu Di

المصدر: Journal of Pharmacological Sciences, Vol 148, Iss 1, Pp 19-30 (2022)

الوصف: Hepatic ischemia/reperfusion (I/R) injury contributes to morbidity and mortality during liver resection or transplantation, with limited effective treatments available. Here, we investigated the potential benefits and underlying mechanisms of pterostilbene (Pt), a natural component of blueberries and grapes, in preventing hepatic I/R injury. Male C57BL/6 mice subjected to partial warm hepatic I/R and human hepatocyte cell line L02 cells exposed to anoxia/reoxygenation (A/R) were used as in vivo and in vitro models, respectively. Our findings showed that pretreatment with Pt ameliorated hepatic I/R injury by improving liver histology, decreasing hepatocyte apoptosis, and reducing plasma ALT and AST levels. Likewise, cell apoptosis, mitochondrial membrane dysfunction, and mitochondrial ROS overproduction in L02 cells triggered by the A/R challenge in vitro were reduced due to Pt administration. Mechanistically, Pt treatment efficiently enhanced mitophagy and upregulated PINK1, Parkin, and LC3B expression. Notably, the protective effect of Pt was largely abrogated after cells were transfected with PINK1 siRNA. Moreover, Pt pretreatment promoted hepatocyte proliferation and liver regeneration in the late phase of hepatic I/R. In conclusion, our findings provide evidence that Pt exerts hepatoprotective effects in hepatic I/R injury by upregulating PINK1-mediated mitophagy.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6e94a469a71dc0eac96e0f9b510a51fc
http://www.sciencedirect.com/science/article/pii/S1347861321000918

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6

Role of vasodilation in liver regeneration and health

المؤلفون: Eckhard Lammert, Linda Große-Segerath

المصدر: Biological Chemistry. 402:1009-1019

الوصف: Recently, we have shown that an enhanced blood flow through the liver triggers hepatocyte proliferation and thereby liver growth. In this review, we first explain the literature on hepatic blood flow and its changes after partial hepatectomy (PHx), before we present the different steps of liver regeneration that take place right after the initial hemodynamic changes induced by PHx. Those parts of the molecular mechanisms governing liver regeneration, which are directly associated with the hepatic vascular system, are subsequently reviewed. These include β1 integrin-dependent mechanotransduction in liver sinusoidal endothelial cells (LSECs), triggering mechanically-induced activation of the vascular endothelial growth factor receptor-3 (VEGFR3) and matrix metalloproteinase-9 (MMP9) as well as release of growth-promoting angiocrine signals. Finally, we speculate how advanced age and obesity negatively affect the hepatic vasculature and thus liver regeneration and health, and we conclude our review with some recent technical progress in the clinic that employs liver perfusion. In sum, the mechano-elastic properties and alterations of the hepatic vasculature are key to better understand and influence liver health, regeneration, and disease.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::57be06c8cddc313121bc948700dc5316
https://doi.org/10.1515/hsz-2021-0155

7

Loss of Claudin-3 Impairs Hepatic Metabolism, Biliary Barrier Function, and Cell Proliferation in the Murine Liver

المؤلفون: Adolfo Odriozola, Mariana Castro Dias, Daniel Candinas, Tural Yarahmadov, Fadi Jebbawi, Mikio Furuse, Benoît Zuber, Alex Odermatt, Cristina Gómez Castellà, Urban Deutsch, Adrian Keogh, Riccardo Tombolini, Deborah Stroka, Britta Engelhardt, Daniel Sánchez-Taltavull, Felix Alexander Baier

المصدر: Cellular and Molecular Gastroenterology and Hepatology, Vol 12, Iss 2, Pp 745-767 (2021)
Cellular and Molecular Gastroenterology and Hepatology
Baier, Felix Alexander; Sánchez-Taltavull, Daniel; Yarahmadov, Tural; Castellà, Cristina Gómez; Jebbawi, Fadi; Keogh, Adrian; Tombolini, Riccardo; Odriozola, Adolfo; Castro Dias, Mariana; Deutsch, Urban; Furuse, Mikio; Engelhardt, Britta; Zuber, Benoît; Odermatt, Alex; Candinas, Daniel; Keogh-Stroka, Deborah M. (2021). Loss of claudin-3 impairs hepatic metabolism, biliary barrier function and cell proliferation in the murine liver. Cellular and molecular gastroenterology and hepatology, 12(2), pp. 745-767. Elsevier 10.1016/j.jcmgh.2021.04.003 <http://dx.doi.org/10.1016/j.jcmgh.2021.04.003>

مصطلحات موضوعية: 0301 basic medicine, Aging, Muricholic acid, RC799-869, Single-Cell RNA Sequencing, chemistry.chemical_compound, 0302 clinical medicine, Claudin-3, UMI, unique molecular identifiers, Original Research, Mice, Knockout, scRNA-seq, single-cell RNA sequencing, CA, cholic acid, Bile acid, Tight junction, Tight Junction, Chemistry, Liver cell, Gastroenterology, Diseases of the digestive system. Gastroenterology, mRNA, messenger RNA, Liver regeneration, 3. Good health, Cell biology, TJ, tight junction, medicine.anatomical_structure, Liver, PHx, partial hepatectomy, Hepatocyte, qPCR, quantitative polymerase chain reaction, 030211 gastroenterology & hepatology, Bile Acid, ALT, alanine-aminotransferase, medicine.drug_class, TCA, taurocholic acid, PBS, phosphate-buffered saline, Taurochenodeoxycholic acid, 610 Medicine & health, Tight Junctions, 03 medical and health sciences, medicine, Animals, Hepatectomy, Claudin, Cell Proliferation, ALP, alkaline phosphatase, Hepatology, Gene Expression Profiling, pHH3, phosphohistone H3, Lipid Metabolism, Liver Regeneration, Mice, Inbred C57BL, 030104 developmental biology, Gene Expression Regulation, Hepatocytes, AST, aspartate-aminotransferase, 570 Life sciences, biology, Bile Ducts, Gene Deletion, DAPI, 4′,6-diamidino-2-phenylindole

الوصف: Background & Aims Tight junctions in the liver are essential to maintain the blood-biliary barrier, however, the functional contribution of individual tight junction proteins to barrier and metabolic homeostasis remains largely unexplored. Here, we describe the cell type–specific expression of tight junction genes in the murine liver, and explore the regulation and functional importance of the transmembrane protein claudin-3 in liver metabolism, barrier function, and cell proliferation. Methods The cell type–specific expression of hepatic tight junction genes is described using our mouse liver single-cell sequencing data set. Differential gene expression in Cldn3-/- and Cldn3+/+ livers was assessed in young and aged mice by RNA sequencing (RNA-seq), and hepatic tissue was analyzed for lipid content and bile acid composition. A surgical model of partial hepatectomy was used to induce liver cell proliferation. Results Claudin-3 is a highly expressed tight junction protein found in the liver and is expressed predominantly in hepatocytes and cholangiocytes. The histology of Cldn3-/- livers showed no overt phenotype, and the canalicular tight junctions appeared intact. Nevertheless, by RNA-seq we detected a down-regulation of metabolic pathways in the livers of Cldn3-/- young and aged mice, as well as a decrease in lipid content and a weakened biliary barrier for primary bile acids, such as taurocholic acid, taurochenodeoxycholic acid, and taurine-conjugated muricholic acid. Coinciding with defects in the biliary barrier and lower lipid metabolism, there was a diminished hepatocyte proliferative response in Cldn3-/- mice after partial hepatectomy. Conclusions Our data show that, in the liver, claudin-3 is necessary to maintain metabolic homeostasis, retention of bile acids, and optimal hepatocyte proliferation during liver regeneration. The RNA-seq data set can be accessed at: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159914.
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URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9bffc6cf475451c7410cb92d0d752071
https://doi.org/10.1016/j.jcmgh.2021.04.003

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8

Determination of the activity of pyruvate kinase isoforms in normal conditions, in toxic liver damage and during the process of its regeneration

المصدر: Health and Ecology Issues. :116-123

مصطلحات موضوعية: chemistry.chemical_compound, Blood serum, chemistry, Regeneration (biology), Liver cell, Hepatotoxin, Carbon tetrachloride, Glycolysis, Pharmacology, Pyruvate kinase, Liver regeneration

الوصف: Objective.To evaluate the activity of pyruvate kinase (PK) isoforms in normal conditions, in toxic damage of the liver and during its regeneration.Materials and methods.An experimental study was carried out on 45 Wistar rats. Toxic liver damage was induced by the intraperitoneal administration of carbon tetrachloride. Mechanical damage was simulated by the surgical resection of the liver. The levels of PK isoforms R/L and M in the blood serum and liver tissue of the laboratory animals were measured with an ELISA test.Results.It has been found that the level of PK isoform M signifcantly increases in chronic toxic liver damage, which may indicate the activation of the processes of liver cell proliferation in response to the damaging effect of hepatotoxin (Mann-Whitney U Test: Z = 2.143; p = 0.032). After liver resection, the level of PK R/L, which characterizes the activation of glycolysis, increased and the level of pyruvate kinase M increased signifcantly, which reﬂected the processes of reparative regeneration in the liver.Conclusion.The serum level of PK isoforms may be used as a laboratory criterion for the activity of reparative regeneration processes, which can be used to evaluate the reparative potential of the liver in case of toxic or mechanical damage, as well as in chronic diffuse diseases.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::6a0297a20a4796be9892b306244d27a9
https://doi.org/10.51523/2708-6011.2021-18-3-14

9

FGF15 improves outcomes after brain dead donor liver transplantation with steatotic and non-steatotic grafts in rats

المؤلفون: José Gulfo, Floriana Rotondo, Cindy G. Avalos de León, Carla Fuster, María Eugenia Cornide-Petronio, Carmen A. Peralta, Mónica B. Jiménez-Castro, Jordi Gracia-Sancho

المصدر: Journal of Hepatology. 73:1131-1143

مصطلحات موضوعية: 0301 basic medicine, Brain Death, medicine.medical_specialty, Receptor complex, medicine.drug_class, medicine.medical_treatment, Delayed Graft Function, Down-Regulation, Liver transplantation, Protective Agents, Cholesterol 7 alpha-hydroxylase, Bile Acids and Salts, Fragile X Mental Retardation Protein, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, medicine, Animals, Intestinal Mucosa, Cholesterol 7-alpha-Hydroxylase, Hepatology, Bile acid, business.industry, FGF15, Intracellular Signaling Peptides and Proteins, Cholic acid, YAP-Signaling Proteins, Liver regeneration, Liver Regeneration, Liver Transplantation, Rats, Fatty Liver, Fibroblast Growth Factors, 030104 developmental biology, Endocrinology, Liver, chemistry, Toxicity, 030211 gastroenterology & hepatology, business, Signal Transduction

الوصف: Background & Aims Donation after brain death (DBD) grafts are associated with reduced graft quality and function post liver transplantation (LT). We aimed to elucidate i) the impact of FGF15 levels on DBD grafts; ii) whether this impact resulted from altered intestinal FXR-FGF15; iii) whether administration of FGF15 to donors after brain death could confer a benefit on graft function post LT; and iv) whether FGF15 affects bile acid (BA) accumulation. Methods Steatotic and non-steatotic grafts from DBD donors and donors without brain death were transplanted in rats. FGF15 was administered alone or combined with either a BA (cholic acid) or a YAP inhibitor. Results Brain death induced intestinal damage and downregulation of FXR. The resulting reduced intestinal FGF15 was associated with low hepatic FGF15 levels, liver damage and regenerative failure. Hepatic FGFR4-Klb – the receptor for FGF15 – was downregulated whereas CYP7A1 was overexpressed, resulting in BA accumulation. FGF15 administration to DBD donors increased hepatic FGFR4-Klb, reduced CYP7A1 and normalized BA levels. The benefit of FGF15 on liver damage was reversed by cholic acid, whereas its positive effect on regeneration was maintained. YAP signaling in DBD donors was activated after FGF15 treatment. When a YAP inhibitor was administered, the benefits of FGF15 on regeneration were abolished, whereas its positive effect on hepatic damage remained. Neither the Hippo-YAP-BA nor the BA-IQGAP1-YAP axis was involved in the benefits of FGF15. Conclusion Alterations in the gut-liver axis contribute to the reduced quality of DBD grafts and the associated pathophysiology of LT. FGF15 pre-treatment in DBD donors protected against damage and promoted cell proliferation. Lay summary After brain death, potential liver donors have reduced intestinal FXR, which is associated with reduced intestinal, circulatory and hepatic levels of FGF15. A similar reduction in the cell-surface receptor complex Fgfr4/Klb is observed, whereas CYP7A1 is overexpressed; together, these molecular events result in the dangerous accumulation of bile acids, leading to damage and regenerative failure in brain dead donor grafts. Herein, we demonstrate that when such donors receive appropriate doses of FGF15, CYP7A1 levels and hepatic bile acid toxicity are reduced, and liver regeneration is promoted.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ed3e212fcbc1bc4c39449558ba6abbd1
https://doi.org/10.1016/j.jhep.2020.05.007

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10

The vascular endothelial growth factor signaling pathway regulates liver sinusoidal endothelial cells during liver regeneration after partial hepatectomy

المؤلفون: Xiaoqian Zhang, Ya-Lei Zhao, Juan Lu, Lanjuan Li

المصدر: Expert Review of Gastroenterology & Hepatology. 15:139-147

الوصف: Liver regeneration after partial hepatectomy is a very complex and well-regulated procedure. It utilizes all liver cell types, which are associated with signaling pathways involving growth factors, cytokines, and stimulatory and inhibitory feedback of several growth-related signals. Liver sinusoidal endothelial cells (LSECs) contribute to liver regeneration after partial hepatectomy. Vascular endothelial growth factor (VEGF) has various functions in LSECs. In this review, we summarize the relationship between VEGF and LSECs involving VEGF regulatory activity in the vascular endothelium.Maintenance of the fenestrated LSEC phenotype requires two VEGF pathways: VEGF stimulated-NO acting through the cGMP pathway and VEGF independent of nitric oxide (NO). The results suggest that VEGF is a key regenerating mediator of LSECs in the partial hepatectomy model. NO-independent pathway was also essential to the maintenance of the LSEC in liver regeneration.Liver regeneration remains a fascinating and significative research field in recent years. The liver involved of molecular pathways except for LSEC-VEGF pathways that make the field of liver further depth studies should be put into effect to elaborate the undetermined confusions, which will be better to understand liver regeneration.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fdea3ce970d7680f33dc5bce79b4a25b
https://doi.org/10.1080/17474124.2020.1815532

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