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Beyond ATP: Metabolite Networks as Regulators of Physiological and Pathological Erythroid Differentiation. 超越 ATP：作为红细胞分化调节器的代谢物网络
IF 5.3 2区 医学
Physiology Pub Date : 2025-01-01 Epub Date: 2024-09-03 DOI: 10.1152/physiol.00035.2024
Axel Joly, Arthur Schott, Ira Phadke, Pedro Gonzalez-Menendez, Sandrina Kinet, Naomi Taylor
{"title":"Beyond ATP: Metabolite Networks as Regulators of Physiological and Pathological Erythroid Differentiation.","authors":"Axel Joly, Arthur Schott, Ira Phadke, Pedro Gonzalez-Menendez, Sandrina Kinet, Naomi Taylor","doi":"10.1152/physiol.00035.2024","DOIUrl":"10.1152/physiol.00035.2024","url":null,"abstract":"<p><p>Hematopoietic stem cells (HSCs) possess the capacity for self-renewal and the sustained production of all mature blood cell lineages. It has been well established that a metabolic rewiring controls the switch of HSCs from a self-renewal state to a more differentiated state, but it is only recently that we have appreciated the importance of metabolic pathways in regulating the commitment of progenitors to distinct hematopoietic lineages. In the context of erythroid differentiation, an extensive network of metabolites, including amino acids, sugars, nucleotides, fatty acids, vitamins, and iron, is required for red blood cell (RBC) maturation. In this review, we highlight the multifaceted roles via which metabolites regulate physiological erythropoiesis as well as the effects of metabolic perturbations on erythroid lineage commitment and differentiation. Of note, the erythroid differentiation process is associated with an exceptional breadth of solute carrier (SLC) metabolite transporter upregulation. Finally, we discuss how recent research, revealing the critical impact of metabolic reprogramming in diseases of disordered and ineffective erythropoiesis, has created opportunities for the development of novel metabolic-centered therapeutic strategies.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Predictors of Inflammation-Mediated Preterm Birth. 炎症引发早产的预测因素
IF 5.3 2区 医学
Physiology Pub Date : 2025-01-01 Epub Date: 2024-08-06 DOI: 10.1152/physiol.00022.2024
Hanah M Georges, Errol R Norwitz, Vikki M Abrahams
{"title":"Predictors of Inflammation-Mediated Preterm Birth.","authors":"Hanah M Georges, Errol R Norwitz, Vikki M Abrahams","doi":"10.1152/physiol.00022.2024","DOIUrl":"10.1152/physiol.00022.2024","url":null,"abstract":"<p><p>Preterm birth remains a worldwide health concern because of ongoing challenges in prediction and prevention. Current predictors are limited by poor performance, need for invasive sampling, and an inability to identify patients in a timely fashion to allow for effective intervention. The multiple etiologies of preterm birth often have an inflammatory component. Thus, a deeper understanding of the inflammatory mechanisms involved in preterm birth may provide opportunities to identify new predictors of preterm birth. This review discusses the multiple etiologies of preterm birth, their links to inflammation, current predictors available, and new directions for the field.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141898670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mechanical Remodeling of Nuclear Biomolecular Condensates. 核生物分子凝聚体的机械重塑。
IF 5.3 2区 医学
Physiology Pub Date : 2025-01-01 Epub Date: 2024-08-07 DOI: 10.1152/physiol.00027.2024
Giulia Soggia, Yasmin ElMaghloob, Annie-Kermen Boromangnaeva, Adel Al Jord
{"title":"Mechanical Remodeling of Nuclear Biomolecular Condensates.","authors":"Giulia Soggia, Yasmin ElMaghloob, Annie-Kermen Boromangnaeva, Adel Al Jord","doi":"10.1152/physiol.00027.2024","DOIUrl":"10.1152/physiol.00027.2024","url":null,"abstract":"<p><p>Organism health relies on cell proliferation, migration, and differentiation. These universal processes depend on cytoplasmic reorganization driven notably by the cytoskeleton and its force-generating motors. Their activity generates forces that mechanically agitate the cell nucleus and its interior. New evidence from reproductive cell biology revealed that these cytoskeletal forces can be tuned to remodel nuclear membraneless compartments, known as biomolecular condensates, and regulate their RNA processing function for the success of subsequent cell division that is critical for fertility. Both cytoskeletal and nuclear condensate reorganization are common to numerous physiological and pathological contexts, raising the possibility that mechanical remodeling of nuclear condensates may be a much broader mechanism regulating their function. Here, we review this newfound mechanism of condensate remodeling and venture into the contexts of health and disease where it may be relevant, with a focus on reproduction, cancer, and premature aging.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141898669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of RANKL Signaling in Bone Homeostasis. rankl信号在骨平衡中的作用。
IF 5.3 2区 医学
Physiology Pub Date : 2025-01-01 Epub Date: 2024-09-10 DOI: 10.1152/physiol.00031.2024
Cristina Sobacchi, Ciro Menale, Laura Crisafulli, Francesca Ficara
{"title":"Role of RANKL Signaling in Bone Homeostasis.","authors":"Cristina Sobacchi, Ciro Menale, Laura Crisafulli, Francesca Ficara","doi":"10.1152/physiol.00031.2024","DOIUrl":"10.1152/physiol.00031.2024","url":null,"abstract":"<p><p>RANKL and its cognate receptor RANK are crucial regulators of bone metabolism in physiological as well as in pathological conditions. Here we go through the works that unveiled the paramount role of this signaling pathway. We focus on the RANKL cytokine, whose alterations are responsible for rare and common bone diseases. We describe recent insights on the regulation of RANKL expression, which provide new hints for the pharmacological regulation of this molecule. Based on the multiple functions exerted by RANKL (within and outside the bone tissue), we advise caution regarding the potential unintended consequences of its inhibition.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142299569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Factors Contributing to Heat Tolerance in Humans and Experimental Models. 导致人类和实验模型耐热性的因素。
IF 5.3 2区 医学
Physiology Pub Date : 2025-01-01 Epub Date: 2024-08-27 DOI: 10.1152/physiol.00028.2024
Orlando Laitano, Kentaro Oki, Nisha Charkoudian
{"title":"Factors Contributing to Heat Tolerance in Humans and Experimental Models.","authors":"Orlando Laitano, Kentaro Oki, Nisha Charkoudian","doi":"10.1152/physiol.00028.2024","DOIUrl":"10.1152/physiol.00028.2024","url":null,"abstract":"<p><p>Understanding physiological mechanisms of tolerance to heat exposure, and potential ways to improve such tolerance, is increasingly important in the context of ongoing climate change. We discuss the concept of heat tolerance in humans and experimental models (primarily rodents), including intracellular mechanisms and improvements in tolerance with heat acclimation.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142074353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Harnessing Deep Learning Methods for Voltage-Gated Ion Channel Drug Discovery. 利用深度学习方法发现电压门控离子通道药物。
IF 5.3 2区 医学
Physiology Pub Date : 2025-01-01 Epub Date: 2024-08-27 DOI: 10.1152/physiol.00029.2024
Diego Lopez-Mateos, Brandon John Harris, Adriana Hernández-González, Kush Narang, Vladimir Yarov-Yarovoy
{"title":"Harnessing Deep Learning Methods for Voltage-Gated Ion Channel Drug Discovery.","authors":"Diego Lopez-Mateos, Brandon John Harris, Adriana Hernández-González, Kush Narang, Vladimir Yarov-Yarovoy","doi":"10.1152/physiol.00029.2024","DOIUrl":"10.1152/physiol.00029.2024","url":null,"abstract":"<p><p>Voltage-gated ion channels (VGICs) are pivotal in regulating electrical activity in excitable cells and are critical pharmaceutical targets for treating many diseases including cardiac arrhythmia and neuropathic pain. Despite their significance, challenges such as achieving target selectivity persist in VGIC drug development. Recent progress in deep learning, particularly diffusion models, has enabled the computational design of protein binders for any clinically relevant protein based solely on its structure. These developments coincide with a surge in experimental structural data for VGICs, providing a rich foundation for computational design efforts. This review explores the recent advancements in computational protein design using deep learning and diffusion methods, focusing on their application in designing protein binders to modulate VGIC activity. We discuss the potential use of these methods to computationally design protein binders targeting different regions of VGICs, including the pore domain, voltage-sensing domains, and interface with auxiliary subunits. We provide a comprehensive overview of the different design scenarios, discuss key structural considerations, and address the practical challenges in developing VGIC-targeting protein binders. By exploring these innovative computational methods, we aim to provide a framework for developing novel strategies that could significantly advance VGIC pharmacology and lead to the discovery of effective and safe therapeutics.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142074354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Low-Grade Chronic Inflammation: a Shared Mechanism for Chronic Diseases. 低度慢性炎症：慢性疾病的共同机制。
IF 5.3 2区 医学
Physiology Pub Date : 2025-01-01 Epub Date: 2024-07-30 DOI: 10.1152/physiol.00021.2024
Mariana Cifuentes, Hugo E Verdejo, Pablo F Castro, Alejandro H Corvalan, Catterina Ferreccio, Andrew F G Quest, Marcelo J Kogan, Sergio Lavandero
{"title":"Low-Grade Chronic Inflammation: a Shared Mechanism for Chronic Diseases.","authors":"Mariana Cifuentes, Hugo E Verdejo, Pablo F Castro, Alejandro H Corvalan, Catterina Ferreccio, Andrew F G Quest, Marcelo J Kogan, Sergio Lavandero","doi":"10.1152/physiol.00021.2024","DOIUrl":"10.1152/physiol.00021.2024","url":null,"abstract":"<p><p>Inflammation is an important physiological response of the organism to restore homeostasis upon pathogenic or damaging stimuli. However, the persistence of the harmful trigger or a deficient resolution of the process can evolve into a state of low-grade, chronic inflammation. This condition is strongly associated with the development of several increasingly prevalent and serious chronic conditions, such as obesity, cancer, and cardiovascular diseases, elevating overall morbidity and mortality worldwide. The current pandemic of chronic diseases underscores the need to address chronic inflammation, its pathogenic mechanisms, and potential preventive measures to limit its current widespread impact. The present review discusses the current knowledge and research gaps regarding the association between low-grade chronic inflammation and chronic diseases, focusing on obesity, cardiovascular diseases, digestive diseases, and cancer. We examine the state of the art in selected aspects of the topic and propose future directions and approaches for the field.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141793887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Olfactory Development and Dysfunction - Involvement of Microglia. 嗅觉发育与功能障碍--小胶质细胞的参与
IF 5.3 2区 医学
Physiology Pub Date : 2024-11-05 DOI: 10.1152/physiol.00037.2024
Sarah J Meller, Charles A Greer
{"title":"Olfactory Development and Dysfunction - Involvement of Microglia.","authors":"Sarah J Meller, Charles A Greer","doi":"10.1152/physiol.00037.2024","DOIUrl":"https://doi.org/10.1152/physiol.00037.2024","url":null,"abstract":"<p><p>Olfactory deficits are increasingly recognized in a variety of neurological, neurodevelopmental, psychiatric and viral diseases. While the pathology underlying olfactory loss is likely to differ across diseases, one shared feature may be an immune response mediated by microglia. Microglia orchestrate the brain's response to environmental insults and maintain neurodevelopmental homeostasis. Here, we explore the potential involvement of microglia in olfactory development and loss in disease. The effects of microglia-mediated immune response during development may be of special relevance to the olfactory system, which is unique in both its vulnerability to environmental insults as well as its extended period of neurogenesis and neuronal migration.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142584749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SUMO regulation of ion channels in health and disease. SUMO 对健康和疾病中离子通道的调控。
IF 5.3 2区 医学
Physiology Pub Date : 2024-11-05 DOI: 10.1152/physiol.00034.2024
Jenna G Connolly, Leigh D Plant
{"title":"SUMO regulation of ion channels in health and disease.","authors":"Jenna G Connolly, Leigh D Plant","doi":"10.1152/physiol.00034.2024","DOIUrl":"https://doi.org/10.1152/physiol.00034.2024","url":null,"abstract":"<p><p>The <u>S</u>mall <u>U</u>biquitin-like <u>Mo</u>difier (SUMO) protein pathway governs a panoply of vital biological processes ranging from cell death, proliferation, differentiation, metabolism, and signal transduction by diversifying the functions, half-lives, and partnerships of target proteins <i>in situ</i>. More recently, SUMOylation has emerged as a key regulator of ion homeostasis and excitability across multiple tissues due to regulation of a plethora of ion channels expressed in a range of tissues subtypes. Altogether, the balance of SUMOylation states amongst relevant ion channels can result in graded biophysical effects that tune excitability and contribute to a range of disease states including cardiac arrythmia, epilepsy, pain transmission, and inflammation. Here, we consolidate these concepts by focusing on the role of ion channel SUMOylation in the central nervous system, peripheral nervous system and the cardiovascular system. In addition, we review what is known about the enigmatic factors that regulate the SUMO pathway and consider the emerging role of small molecule SUMO-modulators as potential therapeutics in a range of diseases.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142584752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Spectrum of Renal "TFEopathies": Flipping the mTOR Switch in Renal Tumorigenesis. TFEopathies "谱系--翻转肾脏肿瘤发生过程中的 mTOR 开关。
IF 5.3 2区 医学
Physiology Pub Date : 2024-11-01 Epub Date: 2024-07-16 DOI: 10.1152/physiol.00026.2024
Nicola Alesi, Kaushal Asrani, Tamara L Lotan, Elizabeth P Henske
{"title":"The Spectrum of Renal \"TFEopathies\": Flipping the mTOR Switch in Renal Tumorigenesis.","authors":"Nicola Alesi, Kaushal Asrani, Tamara L Lotan, Elizabeth P Henske","doi":"10.1152/physiol.00026.2024","DOIUrl":"10.1152/physiol.00026.2024","url":null,"abstract":"<p><p>The mammalian target of Rapamycin complex 1 (mTORC1) is a serine/threonine kinase that couples nutrient and growth factor signaling to the cellular control of metabolism and plays a fundamental role in aberrant proliferation in cancer. mTORC1 has previously been considered an \"on/off\" switch, capable of phosphorylating the entire pool of its substrates when activated. However, recent studies have indicated that mTORC1 may be active toward its canonical substrates, eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1) and S6 kinase (S6K), involved in mRNA translation and protein synthesis, and inactive toward TFEB and TFE3, transcription factors involved in the regulation of lysosome biogenesis, in several pathological contexts. Among these conditions are Birt-Hogg-Dubé syndrome (BHD) and, recently, tuberous sclerosis complex (TSC). Furthermore, increased TFEB and TFE3 nuclear localization in these syndromes, and in translocation renal cell carcinomas (tRCC), drives mTORC1 activity toward the canonical substrates, through the transcriptional activation of the Rag GTPases, thereby positioning TFEB and TFE3 upstream of mTORC1 activity toward 4EBP1 and S6K. The expanding importance of TFEB and TFE3 in the pathogenesis of these renal diseases warrants a novel clinical grouping that we term \"TFEopathies.\" Currently, there are no therapeutic options directly targeting TFEB and TFE3, which represents a challenging and critically required avenue for cancer research.</p>","PeriodicalId":49694,"journal":{"name":"Physiology","volume":" ","pages":"0"},"PeriodicalIF":5.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141621589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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