Immunometabolism (Cobham (Surrey, England))最新文献_第3页

Inflammatory mechanisms in post-traumatic osteoarthritis: a role for CaMKK2. 创伤后骨关节炎的炎症机制：CaMKK2的作用。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-10-16 eCollection Date: 2023-10-01 DOI: 10.1097/IN9.0000000000000031

Keegan C Riggs, Uma Sankar

{"title":"Inflammatory mechanisms in post-traumatic osteoarthritis: a role for CaMKK2.","authors":"Keegan C Riggs, Uma Sankar","doi":"10.1097/IN9.0000000000000031","DOIUrl":"10.1097/IN9.0000000000000031","url":null,"abstract":"Post-traumatic osteoarthritis (PTOA) is a multifactorial disease of the cartilage, synovium, and subchondral bone resulting from direct joint trauma and altered joint mechanics after traumatic injury. There are no current disease-modifying therapies for PTOA, and early surgical interventions focused on stabilizing the joint do not halt disease progression. Chronic pain and functional disability negatively affect the quality of life and take an economic toll on affected patients. While multiple mechanisms are at play in disease progression, joint inflammation is a key contributor. Impact-induced mitochondrial dysfunction and cell death or altered joint mechanics after trauma culminate in inflammatory cytokine release from synoviocytes and chondrocytes, cartilage catabolism, suppression of cartilage anabolism, synovitis, and subchondral bone disease, highlighting the complexity of the disease. Current understanding of the cellular and molecular mechanisms underlying the disease pathology has allowed for the investigation of a variety of therapeutic strategies that target unique apoptotic and/or inflammatory processes in the joint. This review provides a concise overview of the inflammatory and apoptotic mechanisms underlying PTOA pathogenesis and identifies potential therapeutic targets to mitigate disease progression. We highlight Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2), a serine/threonine protein kinase that was recently identified to play a role in murine and human osteoarthritis pathogenesis by coordinating chondrocyte inflammatory responses and apoptosis. Given its additional effects in regulating macrophage inflammatory signaling and bone remodeling, CaMKK2 emerges as a promising disease-modifying therapeutic target against PTOA.","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"5 4","pages":"e00031"},"PeriodicalIF":0.0,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10578519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41241800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Macrophage immunometabolism in diabetes-associated atherosclerosis. 糖尿病相关动脉粥样硬化的巨噬细胞免疫代谢。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-10-16 eCollection Date: 2023-10-01 DOI: 10.1097/IN9.0000000000000032

Bernardo Gindri Dos Santos, Leigh Goedeke

{"title":"Macrophage immunometabolism in diabetes-associated atherosclerosis.","authors":"Bernardo Gindri Dos Santos, Leigh Goedeke","doi":"10.1097/IN9.0000000000000032","DOIUrl":"10.1097/IN9.0000000000000032","url":null,"abstract":"Macrophages play fundamental roles in atherosclerotic plaque formation, growth, and regression. These cells are extremely plastic and perform different immune functions depending on the stimuli they receive. Initial in vitro studies have identified specific metabolic pathways that are crucial for the proper function of pro-inflammatory and pro-resolving macrophages. However, the plaque microenvironment, especially in the context of insulin resistance and type 2 diabetes, constantly challenges macrophages with several simultaneous inflammatory and metabolic stimuli, which may explain why atherosclerosis is accelerated in diabetic patients. In this mini review, we discuss how macrophage mitochondrial function and metabolism of carbohydrates, lipids, and amino acids may be affected by this complex plaque microenvironment and how risk factors associated with type 2 diabetes alter the metabolic rewiring of macrophages and disease progression. We also briefly discuss current challenges in assessing macrophage metabolism and identify future tools and possible strategies to alter macrophage metabolism to improve treatment options for diabetes-associated atherosclerosis.","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"5 4","pages":"e00032"},"PeriodicalIF":0.0,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10578522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41241801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dietary cholesterol in alcohol-associated liver disease. 酒精相关肝病中的膳食胆固醇。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-05-03 eCollection Date: 2023-04-01 DOI: 10.1097/IN9.0000000000000026

Lin Jia

引用次数: 0

Tissue- and temporal-specific roles of extracellular ATP on T cell metabolism and function. 细胞外 ATP 对 T 细胞新陈代谢和功能的作用具有组织和时间特异性。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-05-01 eCollection Date: 2023-04-01 DOI: 10.1097/IN9.0000000000000025

Igor Santiago-Carvalho, Alma Banuelos, Henrique Borges da Silva

引用次数: 0

Peptidoglycan-induced modulation of metabolic and inflammatory responses. 肽聚糖诱导的代谢和炎症反应调节。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-04-28 eCollection Date: 2023-04-01 DOI: 10.1097/IN9.0000000000000024

Andrea J Wolf

{"title":"Peptidoglycan-induced modulation of metabolic and inflammatory responses.","authors":"Andrea J Wolf","doi":"10.1097/IN9.0000000000000024","DOIUrl":"10.1097/IN9.0000000000000024","url":null,"abstract":"Bacterial cell wall peptidoglycan is composed of innate immune ligands and, due to its important structural role, also regulates access to many other innate immune ligands contained within the bacteria. There is a growing body of literature demonstrating how innate immune recognition impacts the metabolic functions of immune cells and how metabolic changes are not only important to inflammatory responses but are often essential. Peptidoglycan is primarily sensed in the context of the whole bacteria during lysosomal degradation; consequently, the innate immune receptors for peptidoglycan are primarily intracellular cytosolic innate immune sensors. However, during bacterial growth, peptidoglycan fragments are shed and can be found in the bloodstream of humans and mice, not only during infection but also derived from the abundant bacterial component of the gut microbiota. These peptidoglycan fragments influence cells throughout the body and are important for regulating inflammation and whole-body metabolic function. Therefore, it is important to understand how peptidoglycan-induced signals in innate immune cells and cells throughout the body interact to regulate how the body responds to both pathogenic and nonpathogenic bacteria. This mini-review will highlight key research regarding how cellular metabolism shifts in response to peptidoglycan and how systemic peptidoglycan sensing impacts whole-body metabolic function.","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"5 2","pages":"e00024"},"PeriodicalIF":0.0,"publicationDate":"2023-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10144284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9398977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Overview of diet and autoimmune demyelinating optic neuritis: a narrative review. 饮食与自身免疫性脱髓鞘性视神经炎概述：叙述性综述。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-04-27 eCollection Date: 2023-04-01 DOI: 10.1097/IN9.0000000000000022

Scott M Plafker, Tyler Titcomb, Katarzyna Zyla-Jackson, Aneta Kolakowska, Terry Wahls

引用次数: 0

Adipose tissue metabolic changes in chronic kidney disease. 慢性肾脏疾病的脂肪组织代谢变化。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-04-01 DOI: 10.1097/IN9.0000000000000023

Eurico Serrano, Prashamsa Shenoy, Maria Paula Martinez Cantarin

{"title":"Adipose tissue metabolic changes in chronic kidney disease.","authors":"Eurico Serrano, Prashamsa Shenoy, Maria Paula Martinez Cantarin","doi":"10.1097/IN9.0000000000000023","DOIUrl":"https://doi.org/10.1097/IN9.0000000000000023","url":null,"abstract":"Adipose tissue is a complex organ whose functions go beyond being an energy reservoir to sustain proper body energy homeostasis. Functioning as an endocrine organ, the adipose tissue has an active role in the body's metabolic balance regulation through several secreted factors generally termed as adipokines. Thus, adipose tissue dysregulation in chronic kidney disease (CKD) can have a deep impact in the pathophysiology of diseases associated with metabolic dysregulation including metabolic syndrome, insulin resistance (IR), atherosclerosis, and even cachexia. CKD is a progressive disorder linked to increased morbidity and mortality. Despite being characterized by renal function loss, CKD is accompanied by metabolic disturbances such as dyslipidemia, protein energy wasting, chronic low-grade inflammation, IR, and lipid redistribution. Thus far, the mechanisms by which these changes occur and the role of adipose tissue in CKD development and progression are unclear. Further understanding of how these factors develop could have implications for the management of CKD by helping identify pharmacological targets to improve CKD outcomes.","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"5 2","pages":"e00023"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10144329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9768471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Mechanisms of continual efferocytosis by macrophages and its role in mitigating atherosclerosis. 巨噬细胞持续排泄的机制及其在减轻动脉粥样硬化中的作用。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-01-23 eCollection Date: 2023-01-01 DOI: 10.1097/IN9.0000000000000017

Dhananjay Kumar, Rajan Pandit, Arif Yurdagul

{"title":"Mechanisms of continual efferocytosis by macrophages and its role in mitigating atherosclerosis.","authors":"Dhananjay Kumar, Rajan Pandit, Arif Yurdagul","doi":"10.1097/IN9.0000000000000017","DOIUrl":"10.1097/IN9.0000000000000017","url":null,"abstract":"Atherosclerotic cardiovascular disease is the leading cause of death worldwide. Rupture-prone atheromas that give rise to myocardial infarction and stroke are characterized by the presence of a necrotic core and a thin fibrous cap. During homeostasis, cellular debris and apoptotic cells are cleared quickly through a process termed \"efferocytosis\". However, clearance of apoptotic cells is significantly compromised in many chronic inflammatory diseases, including atherosclerosis. Emerging evidence suggests that impairments in efferocytosis drive necrotic core formation and contribute significantly to plaque vulnerability. Recently, it has been appreciated that successive rounds of efferocytosis, termed \"continual efferocytosis\", is mechanistically distinct from single efferocytosis and relies heavily on the metabolism and handling of apoptotic cell-derived cargo. In vivo, selective defects in continual efferocytosis drive secondary necrosis, impair inflammation resolution, and worsen atherosclerosis. This Mini Review focuses on our current understanding of the cellular and molecular mechanisms of continual efferocytosis and how dysregulations in this process mediate nonresolving inflammation. We will also discuss possible strategies to enhance efferocytosis when it fails.","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"5 1","pages":"e00017"},"PeriodicalIF":0.0,"publicationDate":"2023-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9869949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10589429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of ApoE-mediated microglial lipid metabolism in brain aging and disease. apoe介导的小胶质脂质代谢在脑衰老和疾病中的作用。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-01-01 DOI: 10.1097/IN9.0000000000000018

Jui-Hung Jimmy Yen, I-Chen Ivorine Yu

{"title":"The role of ApoE-mediated microglial lipid metabolism in brain aging and disease.","authors":"Jui-Hung Jimmy Yen, I-Chen Ivorine Yu","doi":"10.1097/IN9.0000000000000018","DOIUrl":"https://doi.org/10.1097/IN9.0000000000000018","url":null,"abstract":"Microglia are a unique population of immune cells resident in the brain that integrate complex signals and dynamically change phenotypes in response to the brain microenvironment. In recent years, single-cell sequencing analyses have revealed profound cellular heterogeneity and context-specific transcriptional plasticity of microglia during brain development, aging, and disease. Emerging evidence suggests that microglia adapt phenotypic plasticity by flexibly reprogramming cellular metabolism to fulfill distinct immune functions. The control of lipid metabolism is central to the appropriate function and homeostasis of the brain. Microglial lipid metabolism regulated by apolipoprotein E (ApoE), a crucial lipid transporter in the brain, has emerged as a critical player in regulating neuroinflammation. The ApoE gene allelic variant, ε4, is associated with a greater risk for neurodegenerative diseases. In this review, we explore novel discoveries in microglial lipid metabolism mediated by ApoE. We elaborate on the functional impact of perturbed microglial lipid metabolism on the underlying pathogenesis of brain aging and disease.","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"5 1","pages":"e00018"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9869962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9142914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The emerging role of the branched chain aminotransferases, BCATc and BCATm, for anti-tumor T-cell immunity. 支链转氨酶BCATc和BCATm在抗肿瘤t细胞免疫中的新作用。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2023-01-01 DOI: 10.1097/IN9.0000000000000014

Tanner J Wetzel, Sheila C Erfan, Elitsa A Ananieva

{"title":"The emerging role of the branched chain aminotransferases, BCATc and BCATm, for anti-tumor T-cell immunity.","authors":"Tanner J Wetzel, Sheila C Erfan, Elitsa A Ananieva","doi":"10.1097/IN9.0000000000000014","DOIUrl":"https://doi.org/10.1097/IN9.0000000000000014","url":null,"abstract":"Challenges regarding successful immunotherapy are associated with the heterogeneity of tumors and the complex interactions within the surrounding tumor microenvironment (TME), particularly those between immune and tumor cells. Of interest, T cells receive a myriad of environmental signals to elicit differentiation to effector subtypes, which is accompanied by metabolic reprogramming needed to satisfy the high energy and biosynthetic demands of their activated state. However, T cells are subjected to immunosuppressive signals and areas of oxygen and nutrient depletion in the TME, which causes T-cell exhaustion and helps tumor cells escape immune detection. The cytosolic and mitochondrial branched chain amino transferases, BCATc and BCATm, respectively, are responsible for the first step of the branched chain amino acid (BCAA) degradation, of which, metabolites are shunted into various metabolic processes. In recent years, BCAT isoenzymes have been investigated for their role in a variety of cancers found throughout the body; however, a gap of knowledge exists regarding the role BCAT isoenzymes play within immune cells of the TME. The aim of this review is to summarize recent findings about BCAAs and their catabolism at the BCAT step during T-cell metabolic reprogramming and to discuss the BCAT putative role in the anti-tumor immunity of T cells. Not only does this review acknowledges gaps pertaining to BCAA metabolism in the TME but it also identifies the practical application of BCAA metabolism in T cells in response to cancer and spotlights a potential target for pharmacological intervention.","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"5 1","pages":"e00014"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9833117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10534464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3