Pub Date : 2025-09-16DOI: 10.1016/j.mocell.2025.100266
Yuan Shao , Wanli Ren , Hao Dai , Fangli Yang , Xiang Li , Shaoqiang Zhang , Junsong Liu , Xiaobao Yao , Qian Zhao , Xin Sun , Zhiwei Zheng , Chongwen Xu
{"title":"Corrigendum to “SKP2 contributes to AKT activation by ubiquitination degradation of PHLPP1, impedes autophagy, and facilitates the survival of thyroid carcinoma” [Molecules and Cells Volume 46, Issue 6, June 2023, 360-373]","authors":"Yuan Shao , Wanli Ren , Hao Dai , Fangli Yang , Xiang Li , Shaoqiang Zhang , Junsong Liu , Xiaobao Yao , Qian Zhao , Xin Sun , Zhiwei Zheng , Chongwen Xu","doi":"10.1016/j.mocell.2025.100266","DOIUrl":"10.1016/j.mocell.2025.100266","url":null,"abstract":"","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":"48 10","pages":"Article 100266"},"PeriodicalIF":6.5,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-10DOI: 10.1016/j.mocell.2025.100276
Thu-Hang Thi Nghiem , Fedho Kusuma , Jeongmin Park , Yeonsoo Joe , Hun Taeg Chung , Jaeseok Han
Ferroptosis is an iron-dependent, lipid-peroxidation-driven form of regulated cell death that is distinct from apoptosis and necroptosis. Its involvement in various diseases highlights the need for reliable detection strategies. We provide a concise guide for ferroptosis detection, outlining key mechanisms, including iron metabolism, lipid remodeling, and antioxidant failure. Cellular, biochemical, genetic, and morphological methods, including viability assays, lipid reactive oxygen species probes, and electron microscopy, have been used to identify ferroptosis in vitro and in vivo. A multiparametric approach is emphasized to ensure the specificity and reproducibility.
{"title":"Brief guide to detecting ferroptosis","authors":"Thu-Hang Thi Nghiem , Fedho Kusuma , Jeongmin Park , Yeonsoo Joe , Hun Taeg Chung , Jaeseok Han","doi":"10.1016/j.mocell.2025.100276","DOIUrl":"10.1016/j.mocell.2025.100276","url":null,"abstract":"<div><div>Ferroptosis is an iron-dependent, lipid-peroxidation-driven form of regulated cell death that is distinct from apoptosis and necroptosis. Its involvement in various diseases highlights the need for reliable detection strategies. We provide a concise guide for ferroptosis detection, outlining key mechanisms, including iron metabolism, lipid remodeling, and antioxidant failure. Cellular, biochemical, genetic, and morphological methods, including viability assays, lipid reactive oxygen species probes, and electron microscopy, have been used to identify ferroptosis in vitro and in vivo. A multiparametric approach is emphasized to ensure the specificity and reproducibility.</div></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":"48 11","pages":"Article 100276"},"PeriodicalIF":6.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-05DOI: 10.1016/j.mocell.2025.100275
Ji-Won Huh , Kwangcheon Park , Hyun-Sup Song , Seongryong Kim , You-Me Kim
Proper subcellular localization of Toll-like receptors (TLRs) is essential for initiating appropriate innate immune responses against pathogens while avoiding self-reactivity. Unc-93 homolog B1 (UNC93B1) is known to mediate the intracellular trafficking of nucleotide-sensing TLRs such as TLR9 which undergoes rapid internalization into endolysosomes upon reaching the cell surface. We previously demonstrated that UNC93B1 also facilitates the plasma membrane localization of TLR5, a sensor for bacterial flagellin. Unlike TLR9, TLR5 remained stably at the cell surface under steady-state conditions, suggesting the involvement of distinct sorting mechanisms. Using mutagenesis-based approaches, we found that the cytoplasmic domain of TLR5 is required for its surface retention, whereas the cytoplasmic domain of TLR9 is dispensable for internalization. Notably, TLR5 contains polybasic residues in its C-terminal region, absent in other TLRs. Deletion or alanine substitution of these residues led to constitutive endocytosis of TLR5. Conversely, appending the TLR5 C-terminal region to the C-terminus of TLR9 promoted its surface accumulation. Moreover, when the TLR5 C-terminal sequence was fused to a cytosolic protein along with a myristoylation motif, it mediated membrane association of the cytosolic protein in a charge-dependent manner. We further found that this region can directly interact with phosphatidic acid, an anionic phospholipid enriched in the plasma membrane. These findings reveal an electrostatic mechanism by which TLR5 is selectively retained at the plasma membrane, providing new insight into receptor-specific localization of TLRs.
{"title":"Charge-dependent localization of Toll-like receptor 5 at the plasma membrane","authors":"Ji-Won Huh , Kwangcheon Park , Hyun-Sup Song , Seongryong Kim , You-Me Kim","doi":"10.1016/j.mocell.2025.100275","DOIUrl":"10.1016/j.mocell.2025.100275","url":null,"abstract":"<div><div>Proper subcellular localization of Toll-like receptors (TLRs) is essential for initiating appropriate innate immune responses against pathogens while avoiding self-reactivity. Unc-93 homolog B1 (UNC93B1) is known to mediate the intracellular trafficking of nucleotide-sensing TLRs such as TLR9 which undergoes rapid internalization into endolysosomes upon reaching the cell surface. We previously demonstrated that UNC93B1 also facilitates the plasma membrane localization of TLR5, a sensor for bacterial flagellin. Unlike TLR9, TLR5 remained stably at the cell surface under steady-state conditions, suggesting the involvement of distinct sorting mechanisms. Using mutagenesis-based approaches, we found that the cytoplasmic domain of TLR5 is required for its surface retention, whereas the cytoplasmic domain of TLR9 is dispensable for internalization. Notably, TLR5 contains polybasic residues in its C-terminal region, absent in other TLRs. Deletion or alanine substitution of these residues led to constitutive endocytosis of TLR5. Conversely, appending the TLR5 C-terminal region to the C-terminus of TLR9 promoted its surface accumulation. Moreover, when the TLR5 C-terminal sequence was fused to a cytosolic protein along with a myristoylation motif, it mediated membrane association of the cytosolic protein in a charge-dependent manner. We further found that this region can directly interact with phosphatidic acid, an anionic phospholipid enriched in the plasma membrane. These findings reveal an electrostatic mechanism by which TLR5 is selectively retained at the plasma membrane, providing new insight into receptor-specific localization of TLRs.</div></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":"48 11","pages":"Article 100275"},"PeriodicalIF":6.5,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-04DOI: 10.1016/j.mocell.2025.100274
Tae Young Kim , Byoung Dae Lee
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons and the accumulation of misfolded α-synuclein. Current treatments, including dopaminergic medications and deep brain stimulation, provide symptomatic relief but do not halt disease progression. Recent advances in molecular research have enabled the development of disease-modifying strategies targeting key pathogenic mechanisms, such as α-synuclein aggregation, mitochondrial dysfunction, and genetic mutations, including LRRK2 and GBA1. In parallel, pluripotent stem cell-derived dopaminergic neurons have emerged as a scalable and ethically viable source for cell replacement therapy. Early-phase clinical trials have demonstrated the safety and functional integration of these grafts. Ongoing research is now focused on enhancing graft purity, immune compatibility, and anatomical precision, including homotopic transplantation and circuit-level reconstruction. Together, these emerging strategies offer the potential to shift PD treatment paradigms by combining symptomatic control with long-term neural restoration. This review summarizes current therapeutic approaches and highlights recent advances in disease-modifying and regenerative interventions for PD.
{"title":"Current therapeutic strategies in Parkinson’s disease: Future perspectives","authors":"Tae Young Kim , Byoung Dae Lee","doi":"10.1016/j.mocell.2025.100274","DOIUrl":"10.1016/j.mocell.2025.100274","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons and the accumulation of misfolded α-synuclein. Current treatments, including dopaminergic medications and deep brain stimulation, provide symptomatic relief but do not halt disease progression. Recent advances in molecular research have enabled the development of disease-modifying strategies targeting key pathogenic mechanisms, such as α-synuclein aggregation, mitochondrial dysfunction, and genetic mutations, including <em>LRRK2</em> and <em>GBA1</em>. In parallel, pluripotent stem cell-derived dopaminergic neurons have emerged as a scalable and ethically viable source for cell replacement therapy. Early-phase clinical trials have demonstrated the safety and functional integration of these grafts. Ongoing research is now focused on enhancing graft purity, immune compatibility, and anatomical precision, including homotopic transplantation and circuit-level reconstruction. Together, these emerging strategies offer the potential to shift PD treatment paradigms by combining symptomatic control with long-term neural restoration. This review summarizes current therapeutic approaches and highlights recent advances in disease-modifying and regenerative interventions for PD.</div></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":"48 11","pages":"Article 100274"},"PeriodicalIF":6.5,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-18DOI: 10.1016/j.mocell.2025.100256
Sung Eun Hong, Murim Choi, Jeongha Lee
Attaining a complete understanding of the genetic architecture underlying common complex traits is challenging due to the substantial contributions of nongenetic factors and the involvement of numerous influencing genes. Genome-wide association studies (GWAS) have identified novel variants associated with such traits, but our understanding of the molecular genetic mechanisms underlying those associations remains limited. Additionally, variants without significant associations from GWAS can influence gene expression, contributing to individual-level variation in traits. This review summarizes the evolution, advancements in, and practical applications of expression quantitative trait loci analysis. Recent large-scale expression quantitative trait loci studies, often at the single-cell level, provide an opportunity to explain how at least some GWAS variants behave and to elucidate the mechanisms underlying individual-level variations. This approach can further be utilized to identify novel drug targets that are tailored to individuals harboring specific genotypes.
{"title":"Role of expression quantitative trait loci (eQTL) in understanding genetic mechanisms underlying common complex diseases.","authors":"Sung Eun Hong, Murim Choi, Jeongha Lee","doi":"10.1016/j.mocell.2025.100256","DOIUrl":"10.1016/j.mocell.2025.100256","url":null,"abstract":"<p><p>Attaining a complete understanding of the genetic architecture underlying common complex traits is challenging due to the substantial contributions of nongenetic factors and the involvement of numerous influencing genes. Genome-wide association studies (GWAS) have identified novel variants associated with such traits, but our understanding of the molecular genetic mechanisms underlying those associations remains limited. Additionally, variants without significant associations from GWAS can influence gene expression, contributing to individual-level variation in traits. This review summarizes the evolution, advancements in, and practical applications of expression quantitative trait loci analysis. Recent large-scale expression quantitative trait loci studies, often at the single-cell level, provide an opportunity to explain how at least some GWAS variants behave and to elucidate the mechanisms underlying individual-level variations. This approach can further be utilized to identify novel drug targets that are tailored to individuals harboring specific genotypes.</p>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":" ","pages":"100256"},"PeriodicalIF":6.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-18DOI: 10.1016/j.mocell.2025.100255
Junsoo Oh, Yeseul Park, Shinae Park, Og-Geum Woo, Jae-Hoon Lee, Jung-Shin Lee, Taekyung Kim
Protein phosphatase 2A-B56 (PP2A-B56) is a key regulator of mitosis, playing an essential role in maintaining chromosomal stability and ensuring the fidelity of cell division. As a component of the PP2A holoenzyme, the B56 regulatory subunit confers substrate specificity, primarily through interactions with the conserved LxxIxE motif on target proteins. This review highlights the molecular mechanisms by which PP2A-B56 regulates key processes in cell division, including chromosome cohesion and condensation, kinetochore-microtubule attachment, spindle assembly checkpoint silencing, and activation of the anaphase-promoting complex/cyclosome. In meiosis, PP2A-B56 safeguards centromeric cohesion and facilitates the transition between divisions, with recruitment strategies that differ across species. Recent studies also emphasize its role in protecting oocyte quality and fertility by maintaining chromosomal stability. Furthermore, the competition among multiple LxxIxE-containing substrates for PP2A-B56 binding introduces an additional layer of temporal and spatial regulation. Finally, we discuss how perturbations in PP2A-B56 activity contribute to chromosomal instability and tumorigenesis. Understanding of PP2A-B56's substrate recognition and regulatory dynamics provides a framework for therapeutic targeting in disorders involving defective cell division.
{"title":"Phosphatase regulation in cell division: With emphasis on PP2A-B56.","authors":"Junsoo Oh, Yeseul Park, Shinae Park, Og-Geum Woo, Jae-Hoon Lee, Jung-Shin Lee, Taekyung Kim","doi":"10.1016/j.mocell.2025.100255","DOIUrl":"10.1016/j.mocell.2025.100255","url":null,"abstract":"<p><p>Protein phosphatase 2A-B56 (PP2A-B56) is a key regulator of mitosis, playing an essential role in maintaining chromosomal stability and ensuring the fidelity of cell division. As a component of the PP2A holoenzyme, the B56 regulatory subunit confers substrate specificity, primarily through interactions with the conserved LxxIxE motif on target proteins. This review highlights the molecular mechanisms by which PP2A-B56 regulates key processes in cell division, including chromosome cohesion and condensation, kinetochore-microtubule attachment, spindle assembly checkpoint silencing, and activation of the anaphase-promoting complex/cyclosome. In meiosis, PP2A-B56 safeguards centromeric cohesion and facilitates the transition between divisions, with recruitment strategies that differ across species. Recent studies also emphasize its role in protecting oocyte quality and fertility by maintaining chromosomal stability. Furthermore, the competition among multiple LxxIxE-containing substrates for PP2A-B56 binding introduces an additional layer of temporal and spatial regulation. Finally, we discuss how perturbations in PP2A-B56 activity contribute to chromosomal instability and tumorigenesis. Understanding of PP2A-B56's substrate recognition and regulatory dynamics provides a framework for therapeutic targeting in disorders involving defective cell division.</p>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":" ","pages":"100255"},"PeriodicalIF":6.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.mocell.2025.100273
Hyunjin Koo , Minah Jung , Sangwoo Lee , Sangjin Go , Yong-Min Kim
Plant synthetic biology is an emerging field that combines bioinformatics, computational gene circuit design, and plant science. It has the potential to be applied in various areas, including the production of pharmaceuticals, vaccines, biofuels, and various biomaterials, including plant natural products. This review highlights recent advancements in plant synthetic biology, particularly in the development and application of biological parts such as promoters and terminators, which play a crucial role in precise gene expression regulation. Furthermore, this review clarified the identification and utilization of bidirectional promoters, which are essential for gene pyramiding, and the significance of maintaining a balance between promoter and terminator combinations for the stability of transgene expression. Furthermore, large-scale identification of promoters using Assay for Transposase-Accessible Chromatin using sequencing and Self-Transcribing Active Regulatory Region sequencing, as well as deep-learning-based models for predicting promoter regions and their transcriptional activity, are discussed. This review provides insights into the identification and application of bioparts in plant synthetic biology to achieve efficient and precise gene regulation.
{"title":"Identification and application of bioparts for plant synthetic biology","authors":"Hyunjin Koo , Minah Jung , Sangwoo Lee , Sangjin Go , Yong-Min Kim","doi":"10.1016/j.mocell.2025.100273","DOIUrl":"10.1016/j.mocell.2025.100273","url":null,"abstract":"<div><div>Plant synthetic biology is an emerging field that combines bioinformatics, computational gene circuit design, and plant science. It has the potential to be applied in various areas, including the production of pharmaceuticals, vaccines, biofuels, and various biomaterials, including plant natural products. This review highlights recent advancements in plant synthetic biology, particularly in the development and application of biological parts such as promoters and terminators, which play a crucial role in precise gene expression regulation. Furthermore, this review clarified the identification and utilization of bidirectional promoters, which are essential for gene pyramiding, and the significance of maintaining a balance between promoter and terminator combinations for the stability of transgene expression. Furthermore, large-scale identification of promoters using Assay for Transposase-Accessible Chromatin using sequencing and Self-Transcribing Active Regulatory Region sequencing, as well as deep-learning-based models for predicting promoter regions and their transcriptional activity, are discussed. This review provides insights into the identification and application of bioparts in plant synthetic biology to achieve efficient and precise gene regulation.</div></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":"48 10","pages":"Article 100273"},"PeriodicalIF":6.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-30DOI: 10.1016/j.mocell.2025.100272
Enyoung Seo , Sooyeon Park , Inho Park , Jinhyuk Bhin
Somatically acquired genomic rearrangements are common genomic alterations that contribute to malignancy by altering the expression or activity of cancer-related genes in human cancer. Genomic rearrangements play a crucial role in tumor development by contributing to driver events in approximately 25% of cancer patients. Most rearrangements are nonrecurrent and lack functional impact. However, some rearrangements produce functional transcripts and act as cancer drivers that may be therapeutic targets. The growing availability of whole-genome and matched RNA-sequencing data from large patient cohorts offers tremendous opportunities to identify novel, clinically relevant drivers arising from genomic rearrangements. In this review, we summarize current knowledge of driver rearrangements as therapeutic targets and highlight recent discoveries of functional transcripts such as intergenic fusions generated by noncanonical rearrangements. We also discuss computational approaches to decode rearrangement patterns and leverage large-scale whole-genome data to discover novel drivers.
{"title":"Decoding genomic rearrangements for cancer driver discovery","authors":"Enyoung Seo , Sooyeon Park , Inho Park , Jinhyuk Bhin","doi":"10.1016/j.mocell.2025.100272","DOIUrl":"10.1016/j.mocell.2025.100272","url":null,"abstract":"<div><div>Somatically acquired genomic rearrangements are common genomic alterations that contribute to malignancy by altering the expression or activity of cancer-related genes in human cancer. Genomic rearrangements play a crucial role in tumor development by contributing to driver events in approximately 25% of cancer patients. Most rearrangements are nonrecurrent and lack functional impact. However, some rearrangements produce functional transcripts and act as cancer drivers that may be therapeutic targets. The growing availability of whole-genome and matched RNA-sequencing data from large patient cohorts offers tremendous opportunities to identify novel, clinically relevant drivers arising from genomic rearrangements. In this review, we summarize current knowledge of driver rearrangements as therapeutic targets and highlight recent discoveries of functional transcripts such as intergenic fusions generated by noncanonical rearrangements. We also discuss computational approaches to decode rearrangement patterns and leverage large-scale whole-genome data to discover novel drivers.</div></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":"48 11","pages":"Article 100272"},"PeriodicalIF":6.5,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-29DOI: 10.1016/j.mocell.2025.100271
Gahbien Lee , Jiyeon Lee , Greg S.B. Suh , Yangkyun Oh
Systemic nutrient sensing is a fundamental process that aligns nutrient availability with an organism’s metabolic demands. This mini-review explores nutrient sensors in the intestine, pancreas, portal vein, and the brain—organs that detect and convey nutrient status to other tissues via neuronal and hormonal signaling. Unlike oral taste receptors that sense external nutrient inputs, these nutrient sensors monitor post ingestive levels of macronutrients (carbohydrates, proteins, and lipids) and micronutrients (vitamins and essential trace elements such as calcium, magnesium, and zinc) within the body. We describe the specific mechanisms by which each organ discerns fluctuations in nutrient concentration and discuss how these signals integrate into endocrine and neural circuits to maintain whole-body nutrient balance. Finally, by comparing mammalian and invertebrate models such as Drosophila, we offer a comprehensive perspective on how organ-level nutrient sensing upholds metabolic homeostasis across diverse species.
{"title":"Post ingestive systemic nutrient sensing for whole-body homeostasis","authors":"Gahbien Lee , Jiyeon Lee , Greg S.B. Suh , Yangkyun Oh","doi":"10.1016/j.mocell.2025.100271","DOIUrl":"10.1016/j.mocell.2025.100271","url":null,"abstract":"<div><div>Systemic nutrient sensing is a fundamental process that aligns nutrient availability with an organism’s metabolic demands. This mini-review explores nutrient sensors in the intestine, pancreas, portal vein, and the brain—organs that detect and convey nutrient status to other tissues via neuronal and hormonal signaling. Unlike oral taste receptors that sense external nutrient inputs, these nutrient sensors monitor post ingestive levels of macronutrients (carbohydrates, proteins, and lipids) and micronutrients (vitamins and essential trace elements such as calcium, magnesium, and zinc) within the body. We describe the specific mechanisms by which each organ discerns fluctuations in nutrient concentration and discuss how these signals integrate into endocrine and neural circuits to maintain whole-body nutrient balance. Finally, by comparing mammalian and invertebrate models such as <em>Drosophila</em>, we offer a comprehensive perspective on how organ-level nutrient sensing upholds metabolic homeostasis across diverse species.</div></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":"48 11","pages":"Article 100271"},"PeriodicalIF":6.5,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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