Experimental & Molecular Medicine <p><em>Experimental &amp; Molecular Medicine (EMM)&nbsp;</em>is Korea&#39;s first biochemistry journal (founded in 1964) and is relaunched in 1996 as an Open Access, fully peer-reviewed international journal. It is a medical research journal devoted to publishing the latest developments in translational research and the recent discoveries in the biomedical field. Submission is encouraged of papers that involve genetic, molecular and cellular studies of human physiology and diseases. The journal seeks to highlight the improved clinical benefits for human health from experimental and translational research performed using specific molecular tools. Studies that encompass basic discoveries with clinical relevance as well as articles dealing with clear in vivo relevance and novelty will also be welcomed.<em>&nbsp;Experimental &amp; Molecular Medicine&nbsp;</em>is an open access, online-only journal.</p> <p>Topics of particular interest within the journal&#39;s scope include, but are not limited to, those listed below:</p> <ul> <li>Cancer biology</li> <li>Immunology</li> <li>Neuroscience</li> <li>Cardiovascular biology</li> <li>Genetics and genomics</li> <li>Gene therapy</li> <li>Metabolic diseases</li> <li>Stem cells and regenerative medicine</li> <li>Physiology and diseases</li> <li>Molecular Medicine</li> </ul> <p>The journal publishes peer-reviewed Original Articles and Reviews. In addition, Research Summaries are provided for selected articles. Editorial articles are brief comments written by the editor(s) of the journal or by guest editor(s) of Special Features based on the contents of the current issue or topical subjects that fall within the scope of the journal.</p> <p>Reviews can be submitted by authors without invitation but authors are encouraged to submit an abstract of the review to the Editor-in-Chief ([email protected]) to consider for suitability prior to submission of a full article. Submissions of Review articles from outstanding graduate students are also encouraged under the following conditions:</p> <ul> <li>An abstract of the review should be submitted to the Editor-in-Chief ([email protected]) to consider for suitability prior to the submission of a full article</li> <li>The student&#39;s supervisor who has the most expertise in the area being reviewed must be a participatory co-author on the paper</li> <li>The article should encompass a critical assessment of an area: the timeliness of this assessment should be explicitly justified</li> </ul> http://feeds.nature.com/emm/rss/current Nature Publishing Group en © 2025 Macmillan Publishers Limited, part of Springer Nature. All rights reserved. Experimental & Molecular Medicine © 2025 Macmillan Publishers Limited, part of Springer Nature. All rights reserved. [email protected]
  • Experimental & Molecular Medicine https://www.nature.com/uploads/product/emm/rss.gif http://feeds.nature.com/emm/rss/current <![CDATA[Multifaceted roles of CARM1 beyond histone arginine methylation]]> https://www.nature.com/articles/s12276-025-01561-7 <![CDATA[

    Experimental & Molecular Medicine, Published online: 29 October 2025; doi:10.1038/s12276-025-01561-7

    Arginine methylation is a key process in cells, affecting many functions such as gene expression and DNA repair. This study focuses on CARM1, an enzyme involved in this process. Researchers explored the roles of CARM1 beyond its known nuclear functions. They used various experiments, including studies on mice, to understand how CARM1 works in different parts of the cell. CARM1 was initially known for modifying histones to regulate genes. However, it also affects other proteins outside the nucleus, influencing processes such as metabolism and cell structure. The study found that CARM1 can act without its enzyme activity, serving as a scaffold to support other cellular functions. The research highlights the potential of CARM1 as a target for treating diseases such as cancer. By developing inhibitors and new technologies such as proteolysis-targeting chimeras, scientists aim to block both its enzymatic and nonenzymatic roles.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.]]> <![CDATA[Multifaceted roles of CARM1 beyond histone arginine methylation]]> Yena ChoYong Kee Kim doi:10.1038/s12276-025-01561-7 Experimental & Molecular Medicine, Published online: 2025-10-29; | doi:10.1038/s12276-025-01561-7 2025-10-29 Experimental & Molecular Medicine 10.1038/s12276-025-01561-7 https://www.nature.com/articles/s12276-025-01561-7 <![CDATA[TET1 loss propels the development of hyperthyroidism by remodeling histone modifications of <i>PAX8</i> promoter]]> https://www.nature.com/articles/s12276-025-01566-2 <![CDATA[

    Experimental & Molecular Medicine, Published online: 29 October 2025; doi:10.1038/s12276-025-01566-2

    Hyperthyroidism is a condition in which the thyroid gland produces too many hormones, leading to symptoms such as weight loss and irritability. Here scientists are exploring the role of a protein called TET1 in thyroid function. TET1 is known for its role in modifying DNA, which can affect how genes are turned on or off. In this study, researchers investigated whether TET1 influences thyroid activity. They used mice that were genetically modified to lack TET1 specifically in their thyroid glands. These mice showed signs of hyperthyroidism such as increased thyroid hormone levels and faster metabolism. The researchers found that TET1 normally helps suppress the activity of certain genes involved in thyroid hormone production by interacting with other proteins that modify DNA structure. This study suggests that TET1 plays a crucial role in regulating thyroid function and that its absence can lead to hyperthyroidism.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.]]>
    <![CDATA[TET1 loss propels the development of hyperthyroidism by remodeling histone modifications of <i>PAX8</i> promoter]]> Hui DangYan LiuYe ZhouMengjun SuiYubo WangWei QiangFang SuiYan ZhangHongxin CaoXiaoyan WuMeiju JiPeng Hou doi:10.1038/s12276-025-01566-2 Experimental & Molecular Medicine, Published online: 2025-10-29; | doi:10.1038/s12276-025-01566-2 2025-10-29 Experimental & Molecular Medicine 10.1038/s12276-025-01566-2 https://www.nature.com/articles/s12276-025-01566-2
    <![CDATA[The multifaceted role of hair as a biospecimen: recent advances in precision medicine and forensic science]]> https://www.nature.com/articles/s12276-025-01548-4 <![CDATA[

    Experimental & Molecular Medicine, Published online: 27 October 2025; doi:10.1038/s12276-025-01548-4

    Hair is a simple yet valuable sample used in many fields such as medicine, cosmetics and forensics. It is easy to collect and store, making it useful for studying diseases and environmental exposures. This study aims to address how hair can be better used in precision medicine and diagnostics. Researchers have found that hair can help detect diseases such as cancer and monitor drug levels in patients. They use advanced techniques including mass spectrometry (a method to measure molecules) to analyze hair samples. This helps in understanding how drugs are absorbed and how diseases progress over time. Hair analysis can also reveal exposure to toxins and stress levels by measuring substances stored in the hair over months. The study concludes that hair is a promising tool for personalized healthcare, offering insights into long-term health conditions.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.]]>
    <![CDATA[The multifaceted role of hair as a biospecimen: recent advances in precision medicine and forensic science]]> Sunil S. AdavKee Woei Ng doi:10.1038/s12276-025-01548-4 Experimental & Molecular Medicine, Published online: 2025-10-27; | doi:10.1038/s12276-025-01548-4 2025-10-27 Experimental & Molecular Medicine 10.1038/s12276-025-01548-4 https://www.nature.com/articles/s12276-025-01548-4
    <![CDATA[Exploring mitophagy levels in <i>Drosophila</i> Malpighian tubules unveils the pivotal role of mitophagy in kidney function and diabetic kidney disease]]> https://www.nature.com/articles/s12276-025-01558-2 <![CDATA[

    Experimental & Molecular Medicine, Published online: 23 October 2025; doi:10.1038/s12276-025-01558-2

    Mitophagy is a process that removes damaged mitochondria to keep cells healthy. This study looks at how mitophagy works in the kidneys using fruit flies, which have similar kidney-like structures called Malpighian tubules. Here researchers used a special protein called mt-Keima to measure mitophagy in these tubules. They found that mitophagy is crucial for the function of the tubules. When mitophagy was reduced, the tubules did not work well, especially under conditions mimicking diabetic kidney disease (DKD). The study used a high-sugar diet to create a DKD model in flies, which led to decreased mitophagy and kidney dysfunction. However, a new compound called PDE701 increased mitophagy and improved kidney function in these flies. The findings suggest that boosting mitophagy could help treat kidney diseases such as DKD.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.]]>
    <![CDATA[Exploring mitophagy levels in <i>Drosophila</i> Malpighian tubules unveils the pivotal role of mitophagy in kidney function and diabetic kidney disease]]> Kang-Min LeeJihun KimHye Lim JungYoung Yeon KimJihoon LeeYeon-Ju LeeEunhee YooHyi-Seung LeeJeanho Yun doi:10.1038/s12276-025-01558-2 Experimental & Molecular Medicine, Published online: 2025-10-23; | doi:10.1038/s12276-025-01558-2 2025-10-23 Experimental & Molecular Medicine 10.1038/s12276-025-01558-2 https://www.nature.com/articles/s12276-025-01558-2
    <![CDATA[Redox regulation by sulfiredoxin-1: bridging cysteine oxidation and liver disease therapeutics]]> https://www.nature.com/articles/s12276-025-01563-5 <![CDATA[

    Experimental & Molecular Medicine, Published online: 23 October 2025; doi:10.1038/s12276-025-01563-5

    Oxidative stress, an imbalance between harmful molecules called reactive oxygen species and the body’s defenses, contributes to many diseases. A key player in managing this stress is a protein called sulfiredoxin 1 (SRXN1). SRXN1 helps to repair proteins damaged by reactive oxygen species, particularly by reversing a process called cysteine sulfinylation, which can impair protein function. This Review explores SRXN1’s role in liver diseases, highlighting its protective effects on hepatocytes under pathological conditions such as acute liver injury, alcoholic liver disease and liver fibrosis. It does this by maintaining redox balance. Researchers used various methods to study SRXN1’s effects, including examining its interactions with other proteins and its impact on cell survival. Results show that, while SRXN1 protects against liver damage, it also aids cancer cell survival in liver cancer.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.]]>
    <![CDATA[Redox regulation by sulfiredoxin-1: bridging cysteine oxidation and liver disease therapeutics]]> Jong-Won KimMengyun KeDonovan WhitfieldBin YangGu Seob RohWen Xie doi:10.1038/s12276-025-01563-5 Experimental & Molecular Medicine, Published online: 2025-10-23; | doi:10.1038/s12276-025-01563-5 2025-10-23 Experimental & Molecular Medicine 10.1038/s12276-025-01563-5 https://www.nature.com/articles/s12276-025-01563-5
    <![CDATA[The emerging landscape of brain glycosylation: from molecular complexity to therapeutic potential]]> https://www.nature.com/articles/s12276-025-01560-8 <![CDATA[

    Experimental & Molecular Medicine, Published online: 14 October 2025; doi:10.1038/s12276-025-01560-8

    The human brain is a complex organ with over 100 billion cells, including neurons and glial cells. It controls thoughts, emotions and actions through intricate communication systems. This Review explores glycosylation, a process where sugars attach to proteins and lipids, which is crucial for brain function but not well understood. Researchers have used advanced techniques such as mass spectrometry to study glycosylation in the brain. Studies have shown that glycosylation influences brain development, neuronal communication and disease mechanisms. For example, changes in glycosylation have been associated with Alzheimer’s and Parkinson’s diseases. The study highlights the importance of understanding glycosylation for developing new treatments. The researchers conclude that glycosylation is a key player in brain health and disease. Future research could lead to new diagnostic tools and therapies for brain disorders by focusing on glycosylation patterns.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.]]>
    <![CDATA[The emerging landscape of brain glycosylation: from molecular complexity to therapeutic potential]]> Youngsuk SeoJi Eun ParkJae Young YuBoyoung LeeJong Hyuk YoonHyun Joo An doi:10.1038/s12276-025-01560-8 Experimental & Molecular Medicine, Published online: 2025-10-14; | doi:10.1038/s12276-025-01560-8 2025-10-14 Experimental & Molecular Medicine 10.1038/s12276-025-01560-8 https://www.nature.com/articles/s12276-025-01560-8
    <![CDATA[S100A8/9-NLRP3-mediated chronic unresolved inflammation drives cardiac pathologies following invasive pneumococcal disease]]> https://www.nature.com/articles/s12276-025-01552-8 <![CDATA[

    Experimental & Molecular Medicine, Published online: 10 October 2025; doi:10.1038/s12276-025-01552-8

    Hospitalization for community-acquired pneumonia (CAP) can lead to serious heart problems, even after recovery. Researchers explored why this happens. They studied both humans and mice to understand the link between pneumonia and heart problems. The study involved 10 healthy adults and 7 pneumonia patients. Researchers collected blood samples to analyze immune responses. They also used mice to study heart changes after pneumonia. The focus was on inflammation and its role in heart damage. Findings showed that inflammation persists even after the infection clears, leading to heart issues. The study identified a specific inflammatory pathway (S100A8/A9-TLR4-NLRP3) as a key player in this process. The researchers concluded that targeting this inflammation could help prevent heart problems after pneumonia. Future treatments might focus on reducing inflammation to protect the heart in pneumonia survivors.]]>
    <![CDATA[S100A8/9-NLRP3-mediated chronic unresolved inflammation drives cardiac pathologies following invasive pneumococcal disease]]> Sultan TousifDaniel MinassianChao HeBaldeep SinghPrachi UmbarkarArvind Singh BhatiMohammed MohasinNathan ErdmannMin XiePalaniappan SethuCarlos J. OrihuelaHind Lal doi:10.1038/s12276-025-01552-8 Experimental & Molecular Medicine, Published online: 2025-10-10; | doi:10.1038/s12276-025-01552-8 2025-10-10 Experimental & Molecular Medicine 10.1038/s12276-025-01552-8 https://www.nature.com/articles/s12276-025-01552-8
    <![CDATA[Fas apoptotic inhibitor molecule 2 mitigates metabolic dysfunction-associated fatty liver disease through autophagic CRTC2 degradation]]> https://www.nature.com/articles/s12276-025-01559-1 <![CDATA[

    Experimental & Molecular Medicine, Published online: 07 October 2025; doi:10.1038/s12276-025-01559-1

    Metabolic dysfunction-associated fatty liver disease (MAFLD) is a common liver condition affecting many people worldwide. Researchers are looking for new ways to treat MAFLD. A recent study explored the role of a protein called FAIM2 in MAFLD. They found that FAIM2 levels are lower in people with MAFLD, and this protein helps reduce fat buildup in the liver. Researchers used mice and primary hepatocytes to study the function of FAIM2. They discovered that, when FAIM2 is missing, fat and inflammation in the liver increase. However, increasing FAIM2 levels can reduce these issues. FAIM2 works by interacting with another protein, CRTC2, and helps break it down through a process called autophagy. The study suggests that boosting FAIM2 could be a new way to treat MAFLD by reducing fat buildup in the liver.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.]]>
    <![CDATA[Fas apoptotic inhibitor molecule 2 mitigates metabolic dysfunction-associated fatty liver disease through autophagic CRTC2 degradation]]> Yongjie YuSha HuTuo ZhangHongjie ShiDajun LiYongping HuangYu ZhangHaitao WangYufeng HuHong YuGuang-Nian ZhaoPeng Zhang doi:10.1038/s12276-025-01559-1 Experimental & Molecular Medicine, Published online: 2025-10-07; | doi:10.1038/s12276-025-01559-1 2025-10-07 Experimental & Molecular Medicine 10.1038/s12276-025-01559-1 https://www.nature.com/articles/s12276-025-01559-1