BIOMOLECULES & THERAPEUTICS (BIOMOLECULES & THERAPEUTICS)（印刷 ISSN 1976-9148，在线 ISSN 2005-4483）是一份国际性的、同行评审的、开放获取的期刊，涵盖与生物活性分子和治疗相关的药理学和毒理学领域。 1993年创刊为《应用药理学杂志》（ISSN 1225-6110），2008年更名为《BIOMOLECULES & THERAPEUTICS》（BIOMOL THER：缩写形式）（第16卷第1期）。它在一月、三月、五月、七月、九月和十一月出版双月刊。所有手稿都应具有创造性、内容丰富，并有助于新药的开发。发表以下类别的文章：评论文章和研究文章。

Biomolecules and Therapeutics (Print ISSN 1976-9148, Online ISSN 2005-4483) is an international, peer-reviewed, open-access journal that focuses on pharmacology and toxicology related to bioactive molecules and their therapeutic applications. Established in 1993 as the Journal of Applied Pharmacology (ISSN 1225-6110), it was renamed Biomolecules and Therapeutics (BIOMOL THER: abbreviated form) in 2008. The journal publishes six issues per year in January, March, May, July, September, and November. All submitted manuscripts should be innovative, content-rich, and contribute to the development of new drugs. The journal accepts the publication of both review articles and research articles.

《Biomolecules and Therapeutics》（印刷 ISSN 1976-9148，在线 ISSN 2005-4483）是一份国际性的、同行评审的开放获取期刊，专注于生物活性分子及其治疗相关的药理学和毒理学领域。该期刊创刊于1993年，最初名为《应用药理学杂志》（ISSN 1225-6110），并于2008年更名为《Biomolecules and Therapeutics》（BIOMOL THER：缩写形式），目前每年出版六期，分别在一月、三月、五月、七月、九月和十一月发行。所有提交的手稿应具备创新性、内容丰富，并对新药的开发有所贡献。期刊接受评论文章和研究文章的发表。

Biomolecules and Therapeutics

A previous pharmacogenomic analysis identified cromolyn, an anti-allergic drug, as an effective anti-fibrotic agent that acts on hepatocytes and stellate cells. Furthermore, cromolyn was shown to be a G protein-coupled receptor 35 (GPR35) agonist. However, it has not been studied whether anti-fibrotic effects are mediated by GPR35. Therefore, in this study, the role of GPR35 in hepatic fibrosis was investigated through the use of lodoxamide, another anti-allergic drug and a potent GPR35 agonist. Longterm treatment with carbon tetrachloride induced hepatic fibrosis, which was inhibited by treatment with lodoxamide. Furthermore, CID2745687, a specific GPR35 antagonist, reversed lodoxamide-mediated anti-fibrotic effects. In addition, lodoxamide treatment showed significant effects on the mRNA expression of collagen Iα1, collagen Iα2, and TGF-β1 in the extracellular matrix. However, a transforming growth factor α (TGF-α) shedding assay revealed lodoxamide not to be a potent agonist of mouse GPR35 in vitro. Therefore, these results showed anti-fibrotic effects of lodoxamide in mice and raise concerns how lodoxamide protects against liver fibrosis in vivo and whether GPR35 is involved in the action.

Mi-Jeong Kim

Soo-Jin Park

So-Yeon Nam

Dong-Soon Im

Biomolecules & Therapeutics

Lodoxamide Attenuates Hepatic Fibrosis in Mice: Involvement of GPR35

洛多沙胺减轻小鼠肝纤维化：GPR35的参与

genetic analysis of familial forms of AD.However, the blocking of Aβ synthesis does not appear to be effective for reducing the brain Aβ levels as we expected.Recently, the importance of Aβ clearance in AD pathogenesis, especially in late-onset sporadic AD (LOAD) has been raised, and the understanding of Aβ clearance mechanism have provided new therapeutic targets. REVISIT TO THE AMYLOID HYPOTHESISThe Aβ cascade hypothesis of AD was originally proposed (Selkoe, 1991;Hardy and Higgins, 1992) by the theory that accumulation of Aβ, in particular Aβ 1-42 , is the initial trigger for neurodegeneration.However, the chemical nature and the precise biological roles of Aβ in AD pathogenesis have been elusive (Castellani and Smith, 2011).Furthermore, the failure of developing clinically effective disease-modifying drugs has underestimated Aβ-based therapeutic approaches but the genetic studies still strongly place Aβ as a favorable target.Early-onset type of AD (EOAD) occurs as a result of gene mutation involving APP, and presenilin genes (PSEN1, PSEN2).Mutation of these genes showed a common phenomenon of Invited Review

Sang-Sun Yoon

Sangmee Ahn Jo

Mechanisms of Amyloid-β Peptide Clearance: Potential Therapeutic Targets for Alzheimer's Disease

淀粉样β肽清除机制：阿尔茨海默病的潜在治疗靶点

Neurodegenerative diseases (NDDs), characterized by the progressive deterioration of the structure and function of the nervous system, represent a significant global health challenge.Emerging research suggests that the gut microbiota plays a critical role in regulating neurodegeneration via modulation of the gut-brain axis.Probiotics, defined as live microorganisms that confer health benefits to the host, have garnered significant attention owing to their therapeutic potential in NDDs.This review examines the current research trends related to the microbiome-gut-brain axis across various NDDs, highlighting key findings and their implications.Additionally, the effects of specific probiotic strains, including Lactobacillus plantarum, Bifidobacterium breve, and Lactobacillus rhamnosus, on neurodegenerative processes were assessed, focusing on their potential therapeutic benefits.Overall, this review emphasizes the potential of probiotics as promising therapeutic agents for NDDs, underscoring the importance of further investigation into this emerging field.

Jin Hee Kim

Yujin Choi

Seungmin Lee

Myung Sook Oh

Probiotics as Potential Treatments for Neurodegenerative Diseases: a Review of the Evidence from <i>in vivo</i> to Clinical Trial

益生菌作为神经退行性疾病的潜在治疗方法：从体内研究到临床试验的证据综述

Pincha Devage Sameera Madushan Fernando, Mei Jing Piao, Herath Mudiyanselage Udari Lakmini Herath, Kyoung Ah Kang, Kwon-Soo Ha, Sungwook Chae3 and Jin Won Hyun. Biomolecules & Therapeutics -0001;0:. https://doi.org/10.4062/biomolther.2024.053

Pincha Devage Sameera Madushan Fernando

Mei Jing Piao

Herath Mudiyanselage Udari Lakmini Herath

Kyoung Ah Kang

Kwon-Soo Ha

Sungwook Chae

Jin Won Hyun

C-Peptide Ameliorates Particulate Matter 2.5-Induced Skin Cell Apoptosis by Inhibiting NADPH Oxidation

C肽通过抑制NADPH氧化减轻PM2.5诱导的皮肤细胞凋亡

Obesity requires treatment as it is associated with health problems such as type 2 diabetes, hypertension, dyslipidemia, cardiovascular diseases, and some cancers, which increase mortality rates. Achieving sufficient weight loss to reduce obesity-related diseases requires a variety of interventions, including comprehensive lifestyle modification of diet and exercise, change in behavior, anti-obesity medications, and surgery. To date, anti-obesity agents with various mechanisms of action have been developed, and mostly reduce energy intake, resulting in weight loss of about 5% to 10% compared to baseline. Recently developed drugs and those currently under development have been shown to reduce body weight by more than 10% and are expected to reduce obesity-related complications. This article summarizes existing and emerging anti-obesity medications, with a particular focus on those evaluated in clinical trials.

Mi Kyung Kim

Hye Soon Kim

An Overview of Existing and Emerging Weight-Loss Drugs to Target Obesity-Related Complications: Insights from Clinical Trials

现有及新兴减肥药物概述：针对与肥胖相关并发症的临床试验见解

In cancer cells, survival genes contribute to uncontrolled growth and the survival of malignant cells, leading to tumor progression. Neurons are post-mitotic cells, fully differentiated and non-dividing after neurogenesis and survival genes are essential for cellular longevity and proper functioning of the nervous system. This review explores recent research findings regarding the role of survival genes, particularly DX2, in degenerative neuronal tissue cells and cancer cells. Survival gene DX2, an exon 2-deleted splice variant of AIMP2 (aminoacyl-tRNA synthetase-interacting multi-functional protein 2), was found to be overexpressed in various cancer types. The potential of DX2 inhibitors as an anti-cancer drug arises from its unique ability to interact with various oncoproteins, such as KRAS and HSP70. Meanwhile, AIMP2 has been reported as a multifunctional cell death-inducing gene, and survival gene DX2 directly and indirectly inhibits AIMP2-induced cell death. DX2 plays multifaceted survival roles in degenerating neurons via various signaling pathways, including PARP 1, TRAF2, and p53 pathways. It is noteworthy that genes that were previously classified as oncogenes, such as AKT and XBP1, are now being considered as curative transgenes for targeting neurodegenerative diseases. A strategic direction for clinical application of survival genes in neurogenerative disease and in cancer is justified.

Kyunghwa Baek

The Dual Role of Survival Genes in Neurons and Cancer Cells: a Strategic Clinical Application of DX2 in Neurodegenerative Diseases and Cancer

生存基因在神经元和癌细胞中的双重作用：DX2在神经退行性疾病和癌症中的战略性临床应用

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK's role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.

Haeun An

Yerin Jang

Jungin Choi

Juhee Hur

Seojeong Kim

Youngjoo Kwon

New Insights into AMPK, as a Potential Therapeutic Target in Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatic Fibrosis

AMPK 作为代谢功能障碍相关脂肪性肝病和肝纤维化潜在治疗靶点的新见解

Abbreviation	Biomol Ther (Seoul)
Journal Impact	3.03
Quartiles(Global)	PHARMACOLOGY & PHARMACY(Q2)

Publication Information	Publisher: Korean Society of Applied Pharmacology，Publishing cycle: Quarterly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 2008，Proportion of original research papers: 83.05%，Self Citation Rate:6.70%， Gold OA Rate: 81.86%
Average review cycle	网友分享经验：较慢,6-12周
Average recruitment ratio	网友分享经验：容易

Biomolecules and Therapeutics

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Lodoxamide Attenuates Hepatic Fibrosis in Mice: Involvement of GPR35

Mechanisms of Amyloid-β Peptide Clearance: Potential Therapeutic Targets for Alzheimer's Disease

Probiotics as Potential Treatments for Neurodegenerative Diseases: a Review of the Evidence from in vivo to Clinical Trial

C-Peptide Ameliorates Particulate Matter 2.5-Induced Skin Cell Apoptosis by Inhibiting NADPH Oxidation

An Overview of Existing and Emerging Weight-Loss Drugs to Target Obesity-Related Complications: Insights from Clinical Trials

The Dual Role of Survival Genes in Neurons and Cancer Cells: a Strategic Clinical Application of DX2 in Neurodegenerative Diseases and Cancer

New Insights into AMPK, as a Potential Therapeutic Target in Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatic Fibrosis

An Overview of Existing and Emerging Weight-Loss Drugs to Target Obesity-Related Complications: Insights from Clinical Trials

C-Peptide Ameliorates Particulate Matter 2.5-Induced Skin Cell Apoptosis by Inhibiting NADPH Oxidation

Probiotics as Potential Treatments for Neurodegenerative Diseases: a Review of the Evidence from in vivo to Clinical Trial

ISSN	1976-9148, 2005-4483
h-index	56