Submit to CIMB Review for CIMB Propose a Special Issue

Journal Menu

Journal Browser

Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 January 2026) | Viewed by 19655

Share This Special Issue

Special Issue Editors

Dr. Haibo Dong

E-Mail Website
Guest Editor

Center for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA
Interests: fatty liver diseases; cellular redox balance; cell death; inflammation; oxidative stress; autophagy; mitochondrial dysfunction; NAD+ homeostasis
Special Issues, Collections and Topics in MDPI journals

Dr. Wei Guo

E-Mail Website
Guest Editor

Center for Translational Biomedical Research, North Carolina Research Campus, University of North Carolina at Greensboro, Kannapolis, NC 28081, USA
Interests: alcohol-associated liver disease; bile acids metabolism; fatty acids metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce a new Special Issue of Current Issues in Molecular Biology that aims to explore the cellular and molecular mechanisms involved in the development and progression of both non-alcoholic fatty liver disease (NAFLD) and alcohol-associated liver disease (ALD).

NAFLD and ALD are significant contributors to the global burden of liver disease. NAFLD, often associated with metabolic syndrome, obesity, diabetes, and cardiovascular disease, has emerged as the most common cause of chronic liver disease worldwide. ALD, on the other hand, is primarily caused by excessive alcohol consumption and encompasses a wide range of liver conditions, including steatosis, alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. NAFLD and ALD are both steatohepatitic processes and share several common features, yet they differ in many aspects. Therefore, understanding the development and progression of both NAFLD and ALD, in addition to uncovering the underlying cellular and molecular mechanisms, is crucial to advancing our knowledge and developing effective therapeutic strategies for the treatment of these liver diseases.

In this Special Issue, we welcome articles that investigate or summarize the cellular and molecular mechanisms that contribute to the pathogenesis and progression of NAFLD, NASH, ALD, and related diseases. We encourage researchers to explore a broad range of topics, including, but not limited to, impaired lipid metabolism, inflammation, oxidative stress, insulin resistance, genetic/epigenetic modifications, and the interplay between alcohol metabolism and liver injury.

Dr. Haibo Dong
Dr. Wei Guo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

non-alcoholic fatty liver disease (NAFLD)
alcohol-associated liver disease (ALD)
lipotoxicity
bile acid metabolism
novel biomarker identification
organelle dysfunction and communication
inflammation and oxidative stress
cell signaling and cell death pathways
lipid metabolism and dysregulation
epigenetic modifications (DNA/RNA/non-coding RNA)
therapeutic targets and interventions

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (10 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Editorial

Jump to: Research, Review

3 pages, 176 KB

Open AccessEditorial

Editorial for Special Issue: “Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition”

by Wei Guo and Haibo Dong

Curr. Issues Mol. Biol. 2026, 48(3), 288; https://doi.org/10.3390/cimb48030288 - 9 Mar 2026

Viewed by 387

Abstract

The nomenclature for fatty liver diseases, characterized by the accumulation of fat in the liver, has recently been updated by a global consensus of liver organizations and societies for steatotic liver disease (SLD) [...] Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

Research

Jump to: Editorial, Review

14 pages, 858 KB

Open AccessArticle

Circulating MicroRNA Profiling for Phenotypic Stratification in Patients with Metabolic Dysfunction-Associated Fatty Liver Disease: A Candidate-Based Study

by Sumbal Nida, Dilshad Ahmed Khan, Muhammad Amjad Pervez, Nayyar Chaudhry, Mohammad Qaiser Alam Khan and Alveena Younas

Curr. Issues Mol. Biol. 2026, 48(3), 272; https://doi.org/10.3390/cimb48030272 - 4 Mar 2026

Viewed by 610

Abstract

Metabolic dysfunction-associated fatty liver disease (MAFLD) comprises phenotypic subgroups, including type-2 diabetes-associated MAFLD (T2D-MAFLD), obesity-associated MAFLD (OB-MAFLD), and lean MAFLD (L-MAFLD). Emerging evidence indicates that dysregulation of miRNAs plays a key role in MAFLD pathogenesis and progression. This study evaluated the diagnostic accuracy of a plasma miRNA-based signature as a non-invasive biomarker for early detection and phenotypic stratification of MAFLD. A total of 393 MAFLD patients and 109 healthy controls were enrolled. Plasma expression of miR-122, miR-103a, miR-222, miR-15a, miR-34a, miR-192, miR-197, and miR-99a was quantified using Reverse transcription polymerase chain reaction. Compared to controls, MAFLD patients exhibited significant upregulation of miR-122, miR-103a, miR-222, miR-15a, and miR-34a, alongside downregulation of miR-197 and miR-99a. Multinomial logistic regression revealed phenotype-specific associations: miR-103a, miR-34a, and miR-197 with T2D-MAFLD; miR-122, miR-222, and miR-99a with OB-MAFLD; and miR-15a with L-MAFLD. Receiver operating characteristic analysis demonstrated highest individual diagnostic accuracy for miR-197 in T2D-MAFLD (AUC = 0.784), miR-99a in OB-MAFLD (AUC = 0.869), and miR-15a in L-MAFLD (AUC = 0.776). Integrating combined miRNA panels with biochemical markers further improved diagnostic performance and clinical utility, achieving high positive and negative predictive values. In conclusion, plasma miRNA signatures enable phenotype-specific discrimination of MAFLD subtypes and may serve as promising non-invasive tools pending multi-center validation. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

14 pages, 1218 KB

Open AccessArticle

Creatinine/Cystatin C Ratio as a Surrogate Marker for Sarcopenia in Hepatitis-C-Associated Liver Cirrhosis After Achieving a Sustained Virologic Response

by Aritoshi Koizumi, Tadashi Namisaki, Akihiko Shibamoto, Takashi Inoue, Shohei Asada, Takuya Matsuda, Satoshi Iwai, Yuki Tsuji, Yukihisa Fujinaga, Norihisa Nishimura, Shinya Sato, Koh Kitagawa, Kosuke Kaji, Akira Mitoro, Kiyoshi Asada, Hiroaki Takaya, Ryuichi Noguchi and Hitoshi Yoshiji

Curr. Issues Mol. Biol. 2026, 48(2), 222; https://doi.org/10.3390/cimb48020222 - 18 Feb 2026

Viewed by 671

Abstract

The creatinine/cystatin C ratio (CCR) has emerged as a simple surrogate marker for muscle mass. This study aimed to evaluate the clinical utility of CCR in identifying sarcopenia among patients with hepatitis-C-virus-related liver cirrhosis who achieved a sustained virological response following antiviral treatment. In this retrospective study, 111 patients treated at our hospital between 2017 and 2022 were assessed for sarcopenia using the Japan Society of Hepatology criteria, which includes handgrip strength (HGS) and skeletal muscle mass index (SMI) measured via computed tomography. Sarcopenia was diagnosed in 30 patients (27.9%). The median CCR was 0.78 in males and 0.55 in females. Multivariate logistic regression analysis identified CCR < 0.56 as an independent factor associated with sarcopenia. Receiver operating characteristic curve analysis demonstrated good diagnostic performance, with an area under the curve of 0.761 for males and 0.801 for females. Furthermore, overall survival was significantly higher in patients with higher CCR values (>0.65 in males and >0.54 in females). The discriminative ability of CCR was comparable to that of HGS, SMI, and the composite diagnosis of sarcopenia. These findings suggest that CCR is a practical and reliable marker for sarcopenia in this patient population. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

14 pages, 2237 KB

Open AccessArticle

Empagliflozin Attenuates Liver Inflammation and Fibrosis in NAFLD: Evidence from Mendelian Randomization and Mouse Experiments

by Chao Fu, Lijiao Deng, Xiaochan Zhu, Bin Wang, Bin Hu, Huan Xue, Qingxuan Zeng and Yi Zhang

Curr. Issues Mol. Biol. 2025, 47(10), 846; https://doi.org/10.3390/cimb47100846 - 15 Oct 2025

Cited by 2 | Viewed by 1981

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver disorder and a major global health challenge, yet effective pharmacological therapies are lacking. Empagliflozin, a sodium–glucose cotransporter-2 (SGLT2) inhibitor, has shown systemic metabolic and anti-inflammatory benefits, but its liver-specific molecular mechanisms remain incompletely understood. In this study, we evaluated the therapeutic effects of empagliflozin in a diet-induced mouse model of NAFLD, supported by Mendelian randomization analysis. Histological examination, serum biochemistry, and hepatic triglyceride quantification demonstrated that empagliflozin markedly attenuated hepatic steatosis and improved liver injury indices. At the molecular level, empagliflozin suppressed NF-κB-mediated inflammatory signaling and significantly downregulated fibrotic markers including α-SMA and COL1A1, while modulating TIMP-1 and MMP-9 expression. Collectively, these findings reveal that empagliflozin ameliorates NAFLD by inhibiting inflammatory and fibrotic molecular pathways, highlighting its potential as a mechanism-based therapeutic option for NAFLD. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

15 pages, 1218 KB

Open AccessArticle

Genetic Risk of MASLD in Mongolians: Role of PNPLA3 and FTO SNPs

by Yumchinsuren Tsedendorj, Dolgion Daramjav, Yesukhei Enkhbat, Ganchimeg Dondov, Gantogtokh Dashjamts, Enkhmend Khayankhyarvaa, Amin-Erdene Ganzorig, Bolor Ulziitsogt, Tegshjargal Badamjav, Batbold Batsaikhan, Shiirevnyamba Avirmed and Tulgaa Lonjid

Curr. Issues Mol. Biol. 2025, 47(8), 605; https://doi.org/10.3390/cimb47080605 - 1 Aug 2025

Cited by 4 | Viewed by 2148

Abstract

Background: This study aimed to determine the association between PNPLA3 rs738409, rs2896019, and FTO rs9939609, rs17817449 single-nucleotide polymorphisms and the risk of metabolic dysfunction-associated steatotic liver disease (MASLD) in Mongolian individuals. Methods: We conducted a case-control study, enrolling 100 MASLD patients and 50 subjects without MASLD. We used the PCR-RFLP technique on three genotype SNPs (rs738409, rs2896019 in PNPLA3, and rs9939609 in FTO). We analyzed liver function and lipid metabolism parameters in the peripheral blood of study participants. A p-value below 0.05 was considered a statistically significant result. Results: This study, which included 150 participants aged 23 to 75, had a mean age of 46.73 ± 11.45 years, with 40% of participants being male (60 individuals). We observed the rs738409 (G), rs2896019 (G), and rs9939609 (A) alleles at a statistically significantly enhanced frequency in the case group (32.5%, 33%, and 21%) compared to the control group (19%, 25%, and 19%), indicating an increased risk of MASLD. The FTO rs17817449 SNP did not show a significant difference between groups. PNPLA3 rs738409 GC/GG genotype (OR = 2.39, p = 0.019) and FTO rs9939609 AT/AA (OR = 2.55, p = 0.025) genotype showed a significant association with MASLD. In the evaluation of the FTO rs9939609, rs17817449, and PNPLA3 rs738409, rs2896019 single-nucleotide polymorphisms among the research individuals, 18.7% had no SNPs, 15.3% had one SNP, 29.3% had two SNPs, 25.3% had three SNPs, and 11.3% had four SNPs. The risk of MASLD increased significantly for individuals having four SNPs (OR = 4.23, p = 0.007). Conclusions: We found that PNPLA3 rs738409 GC/GG genotype and FTO rs9939609 AT/AA genotype are strongly associated with an increased risk of MASLD. Notably, individuals with a higher rate of SNP number, had a significantly higher risk of MASLD. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

16 pages, 1645 KB

Open AccessArticle

Differential Profiles of Gut Microbiota-Derived Metabolites of Bile Acids and Propionate as Potential Predictors of Depressive Disorder in Women with Morbid Obesity at High Risk of Metabolic Dysfunction-Associated Steatotic Liver Disease—A Pilot Study

by Joanna Michalina Jurek, Belen Xifré, Elena Cristina Rusu, Helena Clavero-Mestres, Razieh Mahmoudian, Carmen Aguilar, David Riesco, Javier Ugarte Chicote, Salomé Martinez, Marga Vives, Fàtima Sabench and Teresa Auguet

Curr. Issues Mol. Biol. 2025, 47(5), 353; https://doi.org/10.3390/cimb47050353 - 12 May 2025

Cited by 1 | Viewed by 3464

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a liver condition linked to cardiometabolic diseases and mental health issues, with studies highlighting disruptions in gut microbiota activity, including bile acid (BA) metabolism. Therefore, the main aim of this exploratory analysis was to assess microbiota-derived metabolites, specifically BAs and short-chain fatty acids (SCFAs), as potential biomarkers of depressive disorder (DD) in women with morbid obesity at MASLD risk. In this pilot study, 33 females with morbid obesity who were scheduled for bariatric surgery were evaluated. Medical and clinical data were collected, and microbial metabolites from pre-surgery blood samples were analyzed. Patients were stratified according to the presence of DD. Analysis with Spearman’s rank test was used to assess correlations and logistic regression models were built to evaluate biomarkers as predictors of DD risk using both receiver operating characteristic (ROC) and precision–recall curves. In this cohort, 30.3% of females were reported to have DD, in addition to significantly elevated levels of certain BAs and SCFAs, including glycodeoxycholic acid (GDCA) and propionate, which were also correlated with some metabolic biomarkers. However, there were no differences in the incidence of MASLD or metabolic syndrome between patients with DD or without. In conclusion, microbiota-derived metabolites such as GDCA and propionate may influence DD risk in females with morbid obesity; however, their potential use as predictive biomarkers should be further investigated to confirm their role in psycho-metabolic conditions. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

19 pages, 4449 KB

Open AccessArticle

Ultra-High-Performance Liquid Chromatography–Tandem Mass Spectrometry and Network Pharmacology Reveal the Mechanisms of Rhodiola crenulata in Improving Non-Alcoholic Fatty Liver Disease

by Xin Zeng, Jianwei Wang, Qinyi Xu, Chengdan Deng, Xi Yi, Shang Wang, Ling Yao and Wei Xiang

Curr. Issues Mol. Biol. 2025, 47(5), 324; https://doi.org/10.3390/cimb47050324 - 1 May 2025

Cited by 1 | Viewed by 1780

Abstract

Rhodiola crenulata (RC) is a traditional herb and functional food that has demonstrated beneficial effects in improving physical function, enhancing work capacity, alleviating fatigue, and preventing altitude sickness. Additionally, RC has shown promising effects in the treatment of non-alcoholic fatty liver disease (NAFLD), although its specific bioactive components and underlying mechanisms remain unclear. In this study, ultra-high-performance liquid chromatography–mass spectrometry (UHPLC-MS) combined with network pharmacology was employed to identify six potential bioactive compounds from the serum of rats treated with RC—Salidroside, Tyrosol, Crenulatin, Catechin gallate, Eriodictyol, and Rhodiooctanoside—that may contribute to its therapeutic effects on NAFLD. The efficacy of these compounds in improving NAFLD was assessed in vitro using HepG2 cells exposed to Palmitic acid (PA), and it was found that Catechin gallate exhibited a significant effect in reducing lipid accumulation in HepG2 cells. Furthermore, based on network pharmacology predictions, molecular docking studies suggested that the primary targets of Catechin gallate in alleviating fatty liver might include ABCB1, DYRK1A, PGD, and FUT4. Molecular dynamics simulations revealed stable binding interactions between Catechin gallate and these four target proteins. This study clarifies the material basis of RC in the treatment of NAFLD and provides a theoretical foundation for the application of RC and Catechin gallate as functional additives for the management of NAFLD. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

17 pages, 10987 KB

Open AccessArticle

Comprehensive Analysis of Differentially Expressed Profiles of mRNA 5-Methylcytosine Modification in Metabolic Dysfunction-Associated Steatotic Liver Disease

by Yueying Yang, E Wang, Bing Zhou, Yan Lu, Xiaoying Ding and Yao Li

Curr. Issues Mol. Biol. 2025, 47(5), 305; https://doi.org/10.3390/cimb47050305 - 26 Apr 2025

Cited by 3 | Viewed by 1251

Abstract

RNA methylation plays a critical role in regulating all aspects of RNA function, which are implicated in the pathogenesis of various human diseases. Recent studies emphasize the role of 5-methylcytosine (m5C), an RNA modification, in key biological functions. Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the leading chronic liver condition globally. However, the relationship between m5C methylation and MASLD remains unclear. This study aimed to investigate m5C modification in a mouse model of MASLD. In this research, using RNA transcriptome sequencing (RNA-Seq) and methylated RNA bisulfite sequencing (RNA-BS-Seq) in leptin receptor-deficient mice, we found that genes associated with hypermethylation were primarily linked to lipid metabolism. We identified 156 overlapping and differentially expressed genes (DEGs) that changed at both the mRNA expression level and the m5C modification level. Among them, 72 genes showed elevated expression and m5C modification. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that these genes were significantly associated with lipid metabolism-related signaling pathways. Our results demonstrate that m5C methylation modifications may play an important role in the development of MASLD. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

Review

Jump to: Editorial, Research

25 pages, 1039 KB

Open AccessReview

Interferon Regulatory Factors in Alcohol-Associated Liver Disease: Cell-Type Programs, Danger Signaling, and Therapeutic Opportunities

by Haibo Dong, Wei Guo and Zhanxiang Zhou

Curr. Issues Mol. Biol. 2026, 48(1), 92; https://doi.org/10.3390/cimb48010092 - 16 Jan 2026

Cited by 1 | Viewed by 1334

Abstract

Alcohol-associated liver disease (ALD) contributes substantially to the global burden of cirrhosis and liver-related mortality, driven by ethanol metabolism, oxidative stress, and dysregulated immune signaling. Despite rapidly growing evidence implicating interferon regulatory factors (IRFs) in ALD pathogenesis, an integrated framework linking ethanol-induced danger signals to cell-type-specific IRF programs is lacking. In this comprehensive review, we summarize current knowledge on IRF-centered signaling networks in ALD, spanning DAMP–PAMP sensing, post-translational IRF regulation, and downstream inflammatory, metabolic, and fibrogenic outcomes across various cell types in the liver, including hepatocytes and immune-related cells such as Kupffer cells, monocyte-derived macrophages, dendritic cells, T cells, hepatic stellate cells (HSC), and neutrophils. We also focus on how ethanol-driven DAMP and PAMP signals activate TLR4, TLR9, and cGAS–STING pathways to engage a coordinated network of IRFs—including IRF1, IRF3, IRF4, IRF5, IRF7, and IRF9—that collectively shape inflammatory, metabolic, and cell-fate programs across hepatic cell populations. We further highlight emerging therapeutic strategies such as STING/TBK1 inhibition, NETosis blockade, IL-22-based epithelial repair, and JAK-STAT modulation that converge on IRF pathways. In summary, this review outlines how IRFs contribute to ALD pathogenesis and discusses the potential implications for the development of targeted therapies. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Figure 1

25 pages, 1538 KB

Open AccessReview

Lipid Hormones at the Intersection of Metabolic Imbalances and Endocrine Disorders

by Maria-Zinaida Dobre, Bogdana Virgolici and Ruxandra Cioarcă-Nedelcu

Curr. Issues Mol. Biol. 2025, 47(7), 565; https://doi.org/10.3390/cimb47070565 - 18 Jul 2025

Cited by 6 | Viewed by 5259

Abstract

Lipid hormone imbalances involving glucocorticoids, thyroid hormones (THs), and sex hormones have widespread metabolic consequences, contributing to the global increase in obesity and insulin resistance. This review examines the complex role of disrupted lipid hormone pathways in the development of metabolic disorders, particularly metabolic dysfunction-associated steatotic liver disease (MASLD). Endocrine disorders such as hypercortisolism, hypothyroidism, and polycystic ovary syndrome (PCOS) are closely linked to MASLD through shared metabolic pathways. Mechanisms include glucocorticoid-induced gluconeogenesis and lipolysis, impaired lipid clearance in hypothyroidism, and the hyperandrogenism-induced downregulation of hepatic low-density lipoprotein (LDL) receptors. PCOS-related factors—such as central obesity, adipocyte hypertrophy, low adiponectin levels, and genetic predisposition—further promote hepatic steatosis. Thyroid dysfunction may also impair the hepatic deiodination of T4, contributing to lipid accumulation and inflammation. Given the overlapping pathophysiology among endocrine, hepatic, and reproductive disorders, multidisciplinary collaboration is essential to optimize diagnosis, treatment, and long-term cardiometabolic outcomes. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition)

► Show Figures

Journal Menu

Journal Browser

Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment, 2nd Edition

Share This Special Issue

Special Issue Editors

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (10 papers)

Editorial

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI