FASEB bioAdvances最新文献

Copper homeostasis; A rapier between mycobacteria and macrophages. 铜稳态;分枝杆菌和巨噬细胞之间的剑。

IF 2.5

FASEB bioAdvances Pub Date : 2024-12-25 eCollection Date: 2025-01-01 DOI: 10.1096/fba.2024-00166

Di Hu, Zisha Yang, Jun-Ai Zhang, Ganbin Liu, Jiang Pi, Junfa Xu, Yan Wang, Yi Zhao

{"title":"Copper homeostasis; A rapier between mycobacteria and macrophages.","authors":"Di Hu, Zisha Yang, Jun-Ai Zhang, Ganbin Liu, Jiang Pi, Junfa Xu, Yan Wang, Yi Zhao","doi":"10.1096/fba.2024-00166","DOIUrl":"10.1096/fba.2024-00166","url":null,"abstract":"Copper is a vital trace element crucial for mediating interactions between Mycobacterium and macrophages. Within these immune cells, copper modulates oxidative stress responses and signaling pathways, enhancing macrophage immune functions and facilitating Mycobacterium clearance. Conversely, copper may promote Mycobacterium escape from macrophages through various mechanisms: inhibiting macrophage activity, diminishing phagocytic and bactericidal capacities, and supporting Mycobacterium survival and proliferation. This paradox has intensified research focus on the regulatory role of copper in immune cell-pathogen interactions. Interactions among metal ions can affect Mycobacterium concentration, distribution, and activity within an organism. In this review, we have elucidated the role of copper in these interactions, focusing on the mechanisms by which this metal influences both the immune defense mechanisms of macrophages and the survival strategies of Mycobacterium. The findings suggest that manipulating copper levels could enhance macrophage bactericidal functions and potentially limit Mycobacterium resistance. Therefore, elucidating the regulatory role of copper is pivotal for advancing our understanding of metal homeostasis in immune cell-pathogen dynamics and TB pathogenesis. Furthermore, we recommend further investigation into the role of copper in TB pathogenesis to advance tuberculosis diagnosis and treatment and gain comprehensive insights into metal homeostasis in infectious disease contexts.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"7 1","pages":"e1484"},"PeriodicalIF":2.5,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946988","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

Fluorescent identification of axons, dendrites and soma of neuronal retinal ganglion cells with a genetic marker as a tool for facilitating the study of neurodegeneration. 利用遗传标记对视网膜神经节细胞轴突、树突和胞体进行荧光鉴定，为神经退行性疾病的研究提供工具。

IF 2.5

FASEB bioAdvances Pub Date : 2024-12-16 eCollection Date: 2025-01-01 DOI: 10.1096/fba.2024-00095

Puttipong Sripinun, Wennan Lu, Sergei Nikonov, Suhani Patel, Sarah Hennessy, Tianyuan Yao, Qi N Cui, Brent A Bell, Claire H Mitchell

{"title":"Fluorescent identification of axons, dendrites and soma of neuronal retinal ganglion cells with a genetic marker as a tool for facilitating the study of neurodegeneration.","authors":"Puttipong Sripinun, Wennan Lu, Sergei Nikonov, Suhani Patel, Sarah Hennessy, Tianyuan Yao, Qi N Cui, Brent A Bell, Claire H Mitchell","doi":"10.1096/fba.2024-00095","DOIUrl":"10.1096/fba.2024-00095","url":null,"abstract":"This study characterizes a fluorescent Slc17a6-tdTomato neuronal reporter mouse line with strong labeling of axons throughout the optic nerve, of retinal ganglion cell (RGC) soma in the ganglion cell layer (GCL), and of RGC dendrites in the inner plexiform layer (IPL). The model facilitated assessment of RGC loss in models of degeneration and of RGC detection in mixed neural/glial cultures. The tdTomato signal showed strong overlap with >98% cells immunolabeled with RGC markers RBPMS or BRN3A, consistent with the ubiquitous presence of the vesicular glutamate transporter 2 (VGUT2, SLC17A6) in all RGC subtypes. There was no cross-labeling of ChAT-positive displaced amacrine cells in the GCL, although some signal emanated from the outer plexiform layer, consistent with horizontal cells. The fluorescence allowed rapid screening of RGC loss following optic nerve crush and intraocular pressure (IOP) elevation. The bright fluorescence also enabled non-invasive monitoring of extensive neurite networks and neuron/astrocyte interactions in culture. Robust Ca2+ responses to P2X7R agonist BzATP were detected from fluorescent RGCs using Ca2+-indicator Fura-2. Fluorescence from axons and soma was detected in vivo with a confocal scanning laser ophthalmoscope (cSLO); automatic RGC soma counts enhanced through machine learning approached the numbers found in retinal wholemounts. Controls indicated no impact of Slc17a6-tdTomato expression on light-dependent neuronal function as measured with a microelectrode array (MEA), or on retinal structure as measured with optical coherence tomography (OCT). In summary, the bright fluorescence in axons, dendrites and soma of ~all RGCs in the Slc17a6-tdTomato reporter mouse may facilitate the study of RGCs.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"7 1","pages":"e1478"},"PeriodicalIF":2.5,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947075","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

Diacylglycerol kinase δ is required for skeletal muscle development and regeneration. 二酰基甘油激酶δ是骨骼肌发育和再生所必需的。

IF 2.5

FASEB bioAdvances Pub Date : 2024-11-29 eCollection Date: 2025-01-01 DOI: 10.1096/fba.2024-00134

Hiromichi Sakai, Chiaki Murakami, Mayumi Takechi, Takeshi Urano, Fumio Sakane

{"title":"Diacylglycerol kinase δ is required for skeletal muscle development and regeneration.","authors":"Hiromichi Sakai, Chiaki Murakami, Mayumi Takechi, Takeshi Urano, Fumio Sakane","doi":"10.1096/fba.2024-00134","DOIUrl":"10.1096/fba.2024-00134","url":null,"abstract":"Diacylglycerol kinase δ (DGKδ) phosphorylates diacylglycerol to produce phosphatidic acid. Previously, we demonstrated that down-regulation of DGKδ suppresses the myogenic differentiation of C2C12 myoblasts. However, the myogenic roles of DGKδ in vivo remain unclear. In the present study, we generated DGKδ-conditional knockout mice under the control of the myogenic factor 5 (Myf5) gene promoter, which regulates myogenesis and brown adipogenesis. The knockout mice showed a significant body weight reduction and apparent mass decrease in skeletal muscle, including the tibialis anterior (TA) muscle. Moreover, the thickness of a portion of the myofibers was reduced in DGKδ-deficient TA muscles. However, DGKδ deficiency did not substantially affect brown adipogenesis, suggesting that Myf5-driven DGKδ deficiency mainly affects muscle development. Notably, skeletal muscle injury induced by a cardiotoxin highly up-regulated DGKδ protein expression, and the DGKδ deficiency significantly reduced the thickness of myofibers, the expression levels of myogenic differentiation markers such as embryonic myosin heavy chain and myogenin, and the number of newly formed myofibers containing multiple central nuclei during muscle regeneration. DGKδ was strongly expressed in myogenin-positive satellite cells around the injured myofibers and centronucleated myofibers. These results indicate that DGKδ has important roles in muscle regeneration in activated satellite cells. Moreover, the conditional knockout mice fed with a high-fat diet showed increased fat mass and glucose intolerance. Taken together, these results demonstrate that DGKδ plays crucial roles in skeletal muscle development, regeneration, and function.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"7 1","pages":"e1481"},"PeriodicalIF":2.5,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946990","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 impact of mild episodic ketosis on microglia and hippocampal long-term depression in 5xFAD mice 轻度发作性酮症对5xFAD小鼠小胶质细胞和海马长期抑郁的影响。

IF 2.5

FASEB bioAdvances Pub Date : 2024-10-23 DOI: 10.1096/fba.2024-00123

Jacopo Di Lucente, Jon J. Ramsey, Lee-Way Jin, Izumi Maezawa

{"title":"The impact of mild episodic ketosis on microglia and hippocampal long-term depression in 5xFAD mice","authors":"Jacopo Di Lucente, Jon J. Ramsey, Lee-Way Jin, Izumi Maezawa","doi":"10.1096/fba.2024-00123","DOIUrl":"10.1096/fba.2024-00123","url":null,"abstract":"Ketotherapeutics is a potential metabolic intervention for mitigating dementias; however, its mechanisms and optimal methods of application are not well understood. Our previous in vitro study showed that β-hydroxybutyrate (BHB), a major ketone body, reverses pathological features of amyloid-β oligomer (AβO)-activated microglia. Here we tested the in vivo effects of BHB on microglia and synaptic plasticity in the 5xFAD Alzheimer's disease (AD) mouse model. A short 1-week regimen of daily intraperitoneal injection of BHB (250 mg/kg), which induced brief and mild daily episodic ketosis, was sufficient to mitigate pro-inflammatory microglia activation and reduce brain amyloid-β deposition by enhancing phagocytosis. Remarkably, it mitigated the deficits of hippocampal long-term depression but not long-term potentiation, and this effect was linked to suppression of NLRP3 inflammasome-generated IL-1β. As ketogenic diets are known for poor compliance, our study opens the possibility for alternative approaches such as short-term BHB injections or dietary ketone esters that are less restrictive, potentially safer, and easier for compliance.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"6 12","pages":"581-596"},"PeriodicalIF":2.5,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800084","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

CREB coactivator CRTC1 in melanocortin-4 receptor-expressing cells regulate dietary fat intake 黑色素皮质素-4 受体表达细胞中的 CREB 辅激活因子 CRTC1 可调节饮食中的脂肪摄入量。

IF 2.5

FASEB bioAdvances Pub Date : 2024-10-21 DOI: 10.1096/fba.2024-00111

Shigenobu Matsumura, Miyu Fujisawa, Mizuki Fujiwara, Houko Okayama, Miona Marutani, Eri Nousou, Tsutomu Sasaki, Naoki Harada

{"title":"CREB coactivator CRTC1 in melanocortin-4 receptor-expressing cells regulate dietary fat intake","authors":"Shigenobu Matsumura, Miyu Fujisawa, Mizuki Fujiwara, Houko Okayama, Miona Marutani, Eri Nousou, Tsutomu Sasaki, Naoki Harada","doi":"10.1096/fba.2024-00111","DOIUrl":"10.1096/fba.2024-00111","url":null,"abstract":"Cyclic adenosine monophosphate-response element-binding protein-1-regulated transcription coactivator-1 (CRTC1), a cytoplasmic coactivator that translocates to the nucleus in response to cAMP, is associated with obesity. We previously reported that CRTC1 deficiency in melanocortin-4 receptor (MC4R)-expressing neurons, which regulate appetite and energy metabolism in the brain, causes hyperphagia and obesity under a high-fat diet (HFD). HFD is preferred for mice, and the dietary fat in HFD is the main factor contributing to its palatability. These findings, along with our previous results, suggest that CRTC1 regulates the appetite for dietary fat. Therefore, in this study, we aimed to investigate the dietary fat intake behavior and energy metabolism of MC4R neuron-specific CRTC1 knockout mice fed soybean oil or lard. CRTC1 deficiency increased the intake of soybean oil and significantly increased body weight gain. Furthermore, obesity induced by soybean oil intake was partially due to leptin resistance. No significant changes in soybean oil intake were observed between young CRTC1-deficient and wild-type mice; however, soybean oil intake increased with age. Moreover, lard intake did not significantly affect the body weight. Overall, our findings highlighted the crucial role of CRTC1 in the regulation of spontaneous dietary fat intake. Furthermore, the role of CRTC1 becomes increasingly significant with age.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"6 12","pages":"597-611"},"PeriodicalIF":2.5,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800080","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

Medium-chain fatty acid receptor GPR84 deficiency leads to metabolic homeostasis dysfunction in mice fed high-fat diet 中链脂肪酸受体 GPR84 缺乏会导致高脂饮食小鼠代谢平衡失调

IF 2.5

FASEB bioAdvances Pub Date : 2024-10-17 DOI: 10.1096/fba.2024-00075

Akari Nishida, Ryuji Ohue-Kitano, Yuki Masujima, Hazuki Nonaka, Miki Igarashi, Takako Ikeda, Ikuo Kimura

{"title":"Medium-chain fatty acid receptor GPR84 deficiency leads to metabolic homeostasis dysfunction in mice fed high-fat diet","authors":"Akari Nishida, Ryuji Ohue-Kitano, Yuki Masujima, Hazuki Nonaka, Miki Igarashi, Takako Ikeda, Ikuo Kimura","doi":"10.1096/fba.2024-00075","DOIUrl":"https://doi.org/10.1096/fba.2024-00075","url":null,"abstract":"Overconsumption of food, especially dietary fat, leads to metabolic disorders such as obesity and type 2 diabetes. Long-chain fatty acids, such as palmitoleate are recognized as the risk factors for these disorders owing to their high-energy content and lipotoxicity. In contrast, medium-chain fatty acids (MCFAs) metabolic benefits; however, their underlying molecular mechanisms remain unclear. GPR84 is an MCFA receptor, particularly for C10:0. Although evidence from in vitro experiments and oral administration of C10:0 in mice suggests that GPR84 is related to the metabolic benefits of MCFAs via glucose metabolism, its precise roles in vivo remain unclear. Therefore, the present study investigated whether GPR84 affects glucose metabolism and metabolic function using Gpr84-deficient mice. Although Gpr84-deficient mice were lean and had increased endogenous MCFAs under high-fat diet feeding conditions, they exhibited hyperglycemia and hyperlipidemia along with lower plasma insulin and glucagon-like peptide-1 (GLP-1) levels compared with wild-type mice. Medium-chain triglyceride (C10:0) intake suppressed obesity, and improved plasma glucose and lipid levels, and increased plasma GLP-1 levels in wild-type mice; however, these effects were partially attenuated in Gpr84-deficient mice. Our results indicate that long-term MCFA-mediated GPR84 activation improves the dysfunction of glucose and lipid homeostasis. Our findings may be instrumental for future studies on drug development with GPR84 as a potential target, thereby offering new avenues for the treatment of metabolic disorders like obesity and type 2 diabetes.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"6 11","pages":"526-538"},"PeriodicalIF":2.5,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2024-00075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142596184","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

TMEM182 inhibits myocardial differentiation of human iPS cells by maintaining the activated state of Wnt/β-catenin signaling through an increase in ILK expression TMEM182 通过增加 ILK 的表达维持 Wnt/β-catenin 信号的激活状态，从而抑制人 iPS 细胞的心肌分化

IF 2.5

FASEB bioAdvances Pub Date : 2024-10-14 DOI: 10.1096/fba.2024-00086

Hirofumi Morihara, Shunichi Yokoe, Shigeo Wakabayashi, Shinji Takai

{"title":"TMEM182 inhibits myocardial differentiation of human iPS cells by maintaining the activated state of Wnt/β-catenin signaling through an increase in ILK expression","authors":"Hirofumi Morihara, Shunichi Yokoe, Shigeo Wakabayashi, Shinji Takai","doi":"10.1096/fba.2024-00086","DOIUrl":"https://doi.org/10.1096/fba.2024-00086","url":null,"abstract":"Transmembrane protein 182 (TMEM182) is notably abundant in muscle and adipose tissue, but its role in the heart remains unknown. This study examined the contribution of TMEM182 in the differentiation of human induced pluripotent stem cells (hiPSCs) into cardiomyocytes. For this, we generated hiPSCs overexpressing TMEM182 in a doxycycline-inducible manner and induced their differentiation into cardiomyocytes. On Day 12 of differentiation, expression of the cardiomyocyte markers, TNNT2 and MYH6, was significantly decreased in TMEM182-overexpressing cells. Additionally, we found that phosphorylation of GSK-3β (Ser9) and β-catenin (Ser552) was increased during TMEM182 overexpression, suggesting activation of Wnt/β-catenin signaling. We further focused on integrin-linked kinase (ILK) as the mechanism by which TMEM182 activates Wnt/β-catenin signaling. Evaluation showed that ILK expression was increased in cells overexpressing TMEM182. These results suggest that TMEM182 maintains Wnt/β-catenin signaling in an activated state after mesoderm formation by increasing ILK expression, thereby suppressing hiPSCs differentiation into cardiomyocytes.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"6 11","pages":"565-579"},"PeriodicalIF":2.5,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2024-00086","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142596231","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

New role of calcium-binding fluorescent dye alizarin complexone in detecting permeability from articular cartilage to subchondral bone 钙结合荧光染料茜素络合酮在检测从关节软骨到软骨下骨的渗透性方面的新作用

IF 2.5

FASEB bioAdvances Pub Date : 2024-10-07 DOI: 10.1096/fba.2024-00103

Mingshu Cui, Mengcun Chen, Yanmei Yang, Hamza Akel, Bin Wang

{"title":"New role of calcium-binding fluorescent dye alizarin complexone in detecting permeability from articular cartilage to subchondral bone","authors":"Mingshu Cui, Mengcun Chen, Yanmei Yang, Hamza Akel, Bin Wang","doi":"10.1096/fba.2024-00103","DOIUrl":"https://doi.org/10.1096/fba.2024-00103","url":null,"abstract":"Osteoarthritis (OA) is a chronic degenerative joint disorder characterized by the progressive deterioration of articular cartilage and concomitant alterations in subchondral bone architecture. However, the precise mechanisms underlying the initiation and progression of OA remains poorly understood. In the present study, we explored whether the calcification in the articular cartilage occurred in the early stage of mouse OA model, generated by the surgery destabilization of the medial meniscus (DMM), via the intra-articular injection of alizarin complexone due to its anionic nature for binding calcium-containing crystals. Although we did not observe the calcification in the articular cartilage of early stage of DMM mice, we unexpectedly identified alizarin complexone had the diffusion capacity for detecting the permeability from the articular cartilage to subchondral bone. Our data showed that the diffusion of alizarin complexone from the articular cartilage to calcified cartilage was greater in the early stage of DMM mice than that in sham controls. Additionally, we observed enhanced penetration of alizarin complexone through the periosteum in DMM mice compared to sham mice. In summary, we developed a novel imaging method that offers a valuable tool for further exploration of biochemical communication underlying OA development. Our findings provided new evidence that increased molecular interactions between the articular cartilage and subchondral bone is involved in the pathogenesis of OA progression.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"6 11","pages":"539-554"},"PeriodicalIF":2.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2024-00103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142596364","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

Everything, everywhere, and all at once: A blueprint for supra-organization of core facilities 事无巨细，无处不在，一气呵成：核心设施超组织蓝图

IF 2.5

FASEB bioAdvances Pub Date : 2024-10-07 DOI: 10.1096/fba.2024-00094

Tsiona Elkayam Cohen, Robert Fluhr

{"title":"Everything, everywhere, and all at once: A blueprint for supra-organization of core facilities","authors":"Tsiona Elkayam Cohen, Robert Fluhr","doi":"10.1096/fba.2024-00094","DOIUrl":"https://doi.org/10.1096/fba.2024-00094","url":null,"abstract":"Core facilities are crucial for cutting-edge scientific research in academic institutions, yet they place a significant financial burden on budgets. The viability of these facilities can be improved through cross-institutional collaborations, although initiating and sustaining such partnerships poses challenges. Insights from Israel's recent nationwide organization of core facilities could offer valuable lessons for fostering similar cooperation elsewhere. Despite the chronic shortfall in public research funding, Israeli research institutions were slow to fully embrace infrastructure sharing. This gap led to the creation of the Israel Research Core Facilities (IRCF) in 2022, which linked core facilities across the country through a bottom-up approach. IRCF facilitated the formation of numerous specialized nation-wide networks for intellectual exchange, and supported training workshops and meetings aimed at core technology providers. These initiatives serve dual purposes: they ensure the ongoing advancement of technological capabilities across facilities, regardless of their size or location, and they strengthen the commitment to the IRCF mission by motivating the maintenance of the IRCF database. As a result, a model of “capacity sharing” emerged, connecting all of Israel's core facility centers. This model enhances infrastructure use, supports strategic planning, and fosters growth. With over 450 core experts offering over 1100 scientific services consolidated into a publicly accessible database, IRCF supports research in universities, hospitals, government, and industry. This strategy could act as a model for creating regional core facility organizations to elevate research quality and ensure efficient infrastructure development.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"6 11","pages":"519-525"},"PeriodicalIF":2.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2024-00094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142595668","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

Epigenetic regulation of cardiovascular diseases induced by behavioral and environmental risk factors: Mechanistic, diagnostic, and therapeutic insights 行为和环境风险因素诱发心血管疾病的表观遗传调控：机理、诊断和治疗见解

IF 2.5

FASEB bioAdvances Pub Date : 2024-10-01 DOI: 10.1096/fba.2024-00080

Feifei Bi, Chen Gao, Hongchao Guo

{"title":"Epigenetic regulation of cardiovascular diseases induced by behavioral and environmental risk factors: Mechanistic, diagnostic, and therapeutic insights","authors":"Feifei Bi, Chen Gao, Hongchao Guo","doi":"10.1096/fba.2024-00080","DOIUrl":"https://doi.org/10.1096/fba.2024-00080","url":null,"abstract":"Behavioral and environmental risk factors are critical in the development and progression of cardiovascular disease (CVD). Understanding the molecular mechanisms underlying these risk factors will offer valuable insights for targeted preventive and therapeutic strategies. Epigenetic modifications, including DNA methylation, histone modifications, chromatin remodeling, noncoding RNA (ncRNA) expression, and epitranscriptomic modifications, have emerged as key mediators connecting behavioral and environmental risk factors to CVD risk and progression. These epigenetic alterations can profoundly impact on cardiovascular health and susceptibility to CVD by influencing cellular processes, development, and disease risk over an individual's lifetime and potentially across generations. This review examines how behavioral and environmental risk factors affect CVD risk and health outcomes through epigenetic regulation. We review the epigenetic effects of major behavioral risk factors (such as smoking, alcohol consumption, physical inactivity, unhealthy diet, and obesity) and environmental risk factors (including air and noise pollution) in the context of CVD pathogenesis. Additionally, we explore epigenetic biomarkers, considering their role as causal or surrogate indicators, and discuss epigenetic therapeutics targeting the mechanisms through which these risk factors contribute to CVD. We also address future research directions and challenges in leveraging epigenetic insights to reduce the burden of CVD related to behavioral and environmental factors and improve public health outcomes. This review aims to provide a comprehensive understanding of behavioral and environmental epigenetics in CVD and offer valuable strategies for therapeutic intervention.","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"6 11","pages":"477-502"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2024-00080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142595652","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