Inflammation最新文献

{"title":"4-octyl Itaconate Attenuates Acute Pancreatitis and Associated Lung Injury by Suppressing Ferroptosis in Mice.","authors":"Shimin Lu, Yang Gong, Pengzhan He, Mingming Qi, Weiguo Dong","doi":"10.1007/s10753-025-02256-x","DOIUrl":"https://doi.org/10.1007/s10753-025-02256-x","url":null,"abstract":"<p><p>Acute pancreatitis (AP) is a common gastrointestinal emergency requiring hospitalization. In recent years, several studies have demonstrated a role for 4-octyl itaconate (4-OI) in anti-inflammatory and oxidative stress injury. However, the potential effects of 4-OI in AP have not been investigated. Caerulein and LPS were used to induce experimental AP models in mice and AR42J cells and then studied by histopathology, biochemical, and molecular analysis. Ferroptosis inhibitor ferrostatin-1 effectively improves pancreatic injury and reduces lipid peroxidation products in experimental AP mice. 4-OI treatment significantly alleviated pancreatic and AP-associated lung injury and inflammation in experimental AP mice by inhibiting ferroptosis. The ferroptosis activator Erastin blocked the protective effect of 4-OI against pancreatic injury in AP, validating that 4-OI alleviates pancreatitis injury through ferroptosis. In vitro experiments further confirmed that 4-OI treatment ameliorated AP-induced pancreatic injury by inhibiting ferroptosis. Our study, for the first time, found that 4-OI ameliorates AP and AP-related lung injury by inhibiting ferroptosis in experimental AP mice, providing a new therapeutic target for alleviating AP.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370279","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}

{"title":"Therapeutic Efficacy of Intermittent Ketogenesis in Modulating Adenosine Metabolism, Immune Response, and Seizure Severity in Refractory Temporal Lobe Epilepsy: A Pilot Human Study.","authors":"Seyyed Hossein Khatami, Parsa Alehossein, Sajad Ehtiati, Tayebe Zarei, Farzaneh Salmani, Sadegh Bagherzadeh, Mohammad Razmafrooz, Masoumeh Rajabibazl, Aram Halimi, Mohammad Reza Shahmohammadi, Morteza Faghih Jouibari, Abbas Tafakhori, Saeed Karima","doi":"10.1007/s10753-025-02264-x","DOIUrl":"https://doi.org/10.1007/s10753-025-02264-x","url":null,"abstract":"<p><p>Temporal lobe epilepsy (TLE) is a common neurological disorder characterized by recurrent seizures originating in the temporal lobe, often affecting patients' physical, cognitive, and social well-being. Despite the availability of antiseizure medication (ASMs), approximately 30% of TLE patients exhibit drug-resistant seizures, emphasizing the need for alternative therapeutic approaches. Ketogenic diets, known for their anticonvulsant effects, have shown promise in managing drug-resistant epilepsy. However, their demanding high-fat, low-carbohydrate regimens pose significant adherence challenges. Medium-chain triglyceride (MCT) offers a viable alternative by inducing ketosis periodically without the need for continuous dietary restrictions. This study evaluated seizure severity, biochemical markers, and immune-related factors in TLE patients. The intervention group received neuro-Capridin caprylate and caprate (n-CAP), while the control group did not. Significant findings included increased plasma ATP and adenosine levels in the treatment group, along with higher expression of ADORA1 and CD73 and reduced expression of ADK. Corresponding protein changes were observed, with increased CD73 and decreased ADK levels. Caprylate and Caprate also elevated regulatory T cells and reduced proinflammatory cytokines (TNF-α, IL-6, IL-1β). These changes were associated with significant reductions in seizure severity and frequency. Intermittent ketogenesis through the consumption of Caprylate and Caprate effectively reduced seizures and improved immune and metabolic markers in drug-resistant TLE patients. These findings highlight its potential as a complementary therapy, warranting further exploration of its long-term impact and underlying molecular mechanisms.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370387","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}

{"title":"NOX4 Regulates NLRP3 by Inhibiting the Ubiquitination of LRRC8A to Promote Ferroptosis in Nucleus Pulposus Cells.","authors":"Feng Zhang, Di Cui, Zhaodong Wang, Yifei Li, Kangkang Wang, Haitao Lu, Haiyang Yu, Wei Jiao, Xilong Cui","doi":"10.1007/s10753-025-02253-0","DOIUrl":"https://doi.org/10.1007/s10753-025-02253-0","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) is a significant contributor to low back pain, imposing a considerable socioeconomic burden. Ferroptosis, a novel form of cell death driven by iron and characterized by the accumulation of reactive oxygen species (ROS), has been associated with the progression of IDD. Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) has been widely recognized as a pivotal factor promoting ferroptosis across various diseases; however, its precise role in the pathogenesis of IDD remains incompletely understood. Our experimental findings demonstrated a marked upregulation of NOX4 in degenerated cells, accompanied by elevated ROS levels and a diminished mitochondrial membrane potential, indicating the participation of ferroptosis. Furthermore, the expression of the critical regulatory factor GPX4 was reduced, while ACSL4 levels were significantly increased, further corroborating the involvement of ferroptosis. Functional loss and gain experiments revealed that NOX4 overexpression augmented ferroptosis and ROS production while promoting the secretion of inflammatory cytokines. Subsequent studies indicated that the knockdown of NOX4 could reverse tert-butyl hydroperoxide (TBHP)-induced ferroptosis. Mass spectrometry analysis identified leucine-rich repeat-containing 8A (LRRC8A) as an interacting protein of NOX4, and further validation confirmed that they co-regulate Nod-like receptor pyrin domain-3 (NLRP3) activation through their interaction. Utilizing a rat model of intervertebral disc degeneration, we further corroborated the role of NOX4 in IDD. This study provides theoretical support for the potential application of NOX4-targeting drugs in the treatment of IDD.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255515","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}

{"title":"Prenatal Inflammation Reprograms Hypothalamic-Pituitary-Gonadal Axis Development in Female Rats.","authors":"Vasilina Ignatiuk, Viktoriya Sharova, Liudmila Zakharova","doi":"10.1007/s10753-025-02243-2","DOIUrl":"https://doi.org/10.1007/s10753-025-02243-2","url":null,"abstract":"<p><p>The hypothalamic-pituitary-gonadal (HPG) axis development during critical periods of ontogenesis can be disrupted by stress factors, including in particular maternal immune activation by infectious agents. Bacterial lipopolysaccharide (LPS, E.coli) exposure induces inflammation accompanied by proinflammatory cytokine release. The resulting elevated cytokine levels may lead to a disruption of epigenetic mechanisms regulating HPG axis development and to a reduced fertility in the offspring. This study focused on the long-term effects of prenatal LPS exposure on HPG axis development in female rats and the modulation of such effects by anti-inflammatory drugs: polyclonal IgG and monoclonal anti-IL6-receptor antibodies. LPS exposure on embryonic day 12 led to a decrease in the number of synaptic inputs on gonadotropin-releasing-hormone-producing neurons in the hypothalamus, high levels of follicular atresia, and suppressed steroidogenesis in the ovaries of adult female offspring. IgG treatment or IL6 receptor blockade by monoclonal antibodies 40 minutes after LPS exposure prevented these long-term negative effects of LPS. The data obtained suggest that IL6 is involved in the regulation of HPG axis development.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255519","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}

{"title":"AZD6738 Attenuates LPS-Induced Corneal Inflammation and Fibrosis by Modulating Macrophage Function and Polarization.","authors":"Longxiang Huang, Youfang Luo","doi":"10.1007/s10753-025-02251-2","DOIUrl":"https://doi.org/10.1007/s10753-025-02251-2","url":null,"abstract":"<p><p>This study aimed to evaluate the therapeutic potential of AZD6738, an ATR inhibitor, in LPS-induced bacterial keratitis (BK) by targeting macrophage function and polarization. A murine model of LPS-induced BK was established, with AZD6738 (100 µM) administered subconjunctivally and topically. Corneal opacity, edema, and inflammation were assessed using slit-lamp microscopy and histological analysis. Macrophage infiltration and fibrosis were evaluated via immunofluorescence, qPCR, and Western blotting. In vitro, RAW264.7 cells were treated with 2.5 µM AZD6738 to examine its effects on cell viability, oxidative stress, and inflammation-related gene expression. AZD6738 significantly reduced corneal opacity, thickness, and neovascularization in LPS-treated mice. It suppressed macrophage infiltration, collagen deposition, and pro-inflammatory cytokine expression. In RAW264.7 cells, AZD6738 induced cell death, elevated ROS production, and downregulated inflammatory markers. ATR inhibition mitigated NF-κB activation and modulated macrophage polarization, attenuating M1 pro-inflammatory responses. AZD6738 effectively alleviates LPS-induced corneal inflammation and fibrosis by regulating macrophage function and polarization via the NF-κB signaling pathway. ATR inhibition represents a promising therapeutic strategy for the treatment of corneal inflammation.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189064","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}

{"title":"A Comprehensive Review of Contemporary Bioreactors for Vascular Inflammation Studies.","authors":"Solana Capalbo, Annabella Polyakova, Zayd El Imane, Izza Khan, Toshihisa Kawai, Satoru Shindo, Manuel Salinas","doi":"10.1007/s10753-024-02231-y","DOIUrl":"10.1007/s10753-024-02231-y","url":null,"abstract":"<p><p>The field of vascular biology has advanced significantly with bioreactor systems, which have become essential tools for investigating the mechanisms of vascular inflammatory diseases such as atherosclerosis, vasculitis, and aneurysms. These bioreactors allow researchers to recreate specific vascular environments, providing a controlled setting for studying the effects of blood flow, mechanical stress, and biochemical factors on vascular tissues. Through these systems, researchers can explore how physical and chemical cues contribute to disease processes and cellular responses, enhancing our understanding of disease progression. Bioreactor studies have demonstrated that hemodynamic forces, particularly shear stress, influence endothelial cell behavior and play a role in vascular pathologies. For instance, in atherosclerosis, disturbed flow patterns are associated with endothelial dysfunction and plaque development. By simulating these conditions, bioreactors provide insight into the effects of mechanical forces on vascular wall biology, highlighting how altered flow can contribute to disease. Bioreactors also support studies on the impacts of pulsatile flow and circumferential stress, allowing a closer approximation of physiological environments. Beyond flow dynamics, these systems facilitate investigation into how vascular cells respond to biochemical signals, inflammatory markers, and therapeutic interventions. This integrated approach allows for a more complete picture of the factors involved in vascular disease. Recent advancements, such as vessel-on-a-chip models and artery-mimicking setups, extend the capabilities of bioreactors by enabling researchers to model a broader range of conditions relevant to human physiology. In vasculitis studies, bioreactors help explore immune interactions with endothelial cells, especially with stem cell-derived cells that replicate patient-specific responses. Bioreactors also play a role in vascular tissue engineering, particularly in assessing materials and scaffold-free designs that may reduce inflammation in vascular grafts. These efforts contribute to the ongoing search for more compatible graft materials, with the potential to improve outcomes in clinical applications. This review provides a comprehensive overview of bioreactor technologies applied in vascular inflammation research, examining their designs, applications, and contributions to disease modeling. Organized into sections on bioreactor configurations, flow dynamics, biochemical interactions, and tissue engineering applications, the review concludes by discussing recent innovations and highlighting directions for future research, underscoring the role of bioreactors in bridging laboratory studies with insights into vascular disease.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189056","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}

{"title":"Targeting Lcn2 to Inhibit Myocardial Cell Ferroptosis is a Potential Therapy for Alleviating Septic Cardiomyopathy.","authors":"Cheng Jiang, MingTong Hou, Shougang Sun, Gang Chen, Feng Bai, Shengbao Wang","doi":"10.1007/s10753-025-02250-3","DOIUrl":"https://doi.org/10.1007/s10753-025-02250-3","url":null,"abstract":"<p><p>Septic cardiomyopathy (SCM) represents a key feature of sepsis-associated cardiovascular failure, and ferroptosis is one of the essential causes of septic cardiac dysfunction. In this study, combined with omics analysis and in vivo experiments, we verified the damage of ferroptosis on cardiac tissue in septic mice and mined the target genes that can inhibit ferroptosis in cardiomyocytes. Lipocalin-2 (Lcn2) was identified to be associated with SCM progression via integrated transcriptomic and proteomic analyses. Sepsis was induced by cecal ligation and perforation (CLP) in mice. Ferroptosis and cardiac dysfunction were detected by pathological tissue staining and ELISA. However, after the knockout of Lcn2, cardiomyocyte ferroptosis was significantly suppressed, inflammatory infiltrates were reduced, reactive oxygen species (ROS) levels were lowered, mitochondrial damage was alleviated, and cardiac function was restored in CLP mice. In summary, this study found that Lcn2 can be a potential target for inhibiting ferroptosis in SCM. Targeting Lcn2 can effectively inhibit inflammation, improve mitochondrial dysfunction, inhibit cardiomyocyte ferroptosis, and alleviate SCM.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079692","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}

{"title":"Moxibustion Alleviates Inflammation via SIRT5-mediated Post-translational Modification and Macrophage Polarization.","authors":"Chuan-Yi Zuo, Cheng-Shun Zhang, Han-Xiao Zhang, Chun-Yan Gou, Hong Lei, Feng-Wei Tian, Zhu-Xing Wang, Hai-Yan Yin, Shu-Guang Yu","doi":"10.1007/s10753-025-02239-y","DOIUrl":"https://doi.org/10.1007/s10753-025-02239-y","url":null,"abstract":"<p><p>Macrophage polarisation is influenced by Sirtuin5 (SIRT5), which is crucial for regulating anti-inflammatory processes. Moxibustion, a traditional Chinese medicine therapy, exerts anti-inflammatory effects by altering the succinate/α-ketoglutarate (α-KG) ratio, an indicator of the M1 to M2 macrophage shift. Glutamate dehydrogenase 1 (GLUD1), a key enzyme involved in α-KG production, is desuccinylated by SIRT5. Currently, the potential influence of moxibustion on SIRT5-GLUD1-α-KG-mediated macrophage polarization in inflammatory diseases remains unexplored. C57BL/6 J and Sirt5 knockout mice were used as complete Freund's adjuvant (CFA)-induced adjuvant arthritis models. Moxibustion and acupoint injections of MC3482 were administered. Paw capacity asssays and ELISA were performed to quantify inflammatory effects and the expression of succinate, and α-KG expressions. Flow cytometry (FCM) and immunofluorescence were used to assesss the expression of M1- and M2-like macrophages. LC-MS/MS-based proteomic analysis was performed, and GLUD1 was identified desuccinylated protein associated with SIRT5. Western blotting and immunoprecipitation (IP) were used to detect SIRT5, GLUD1, and succinylated GLUD1expressions. Moxibustion and the SIRT5-mediated desuccinylation inhibitor MC3482 decreased inflammation by increasing the number of M2 macrophages and reducing the number of M1 macrophage in the CFA model. The potential mechanism may be related to the effects of moxibustion and SIRT5 inhibition, which inverted succinate and α-KG levels in the CFA group, resulting in low succinate, high α-KG, and increased GLUD1 succinylation after treatment. These findings suggest that the anti-inflammatory effects moxibustion are related to the impact of macrophage conversion after SIRT5-mediated post-translational modification.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079690","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}

{"title":"Dual Regulation of Nicotine on NLRP3 Inflammasome in Macrophages with the Involvement of Lysosomal Destabilization, ROS and α7nAChR.","authors":"Xiaqing Wu, Yushan Tian, Hongjuan Wang, Huan Chen, Hongwei Hou, Qingyuan Hu","doi":"10.1007/s10753-024-02036-z","DOIUrl":"10.1007/s10753-024-02036-z","url":null,"abstract":"<p><p>Nicotine, the primary alkaloid in tobacco products, has been shown to have immunoregulatory function in at least 20 diseases. The biological mechanism of action of nicotine immunoregulation is complex, resulting in an improvement of some disease states and exacerbation of others. Given the central role of the NLRP3 inflammasome in macrophages among multiple inflammatory diseases, this study examined how nicotine alters NLRP3 inflammasome activation in macrophages. NLRP3 inflammasome activation was examined mechanistically in the context of different nicotine dosages. We show NLRP3 inflammasome activation, apoptosis-associated speck-like protein (ASC) expression, caspase-1 activity and subsequent IL-1β secretion were positively correlated with nicotine in a dose-dependent relationship, and destabilization of lysosomes and ROS production were also involved. At high concentrations of nicotine surpassing 0.25 mM, NLRP3 inflammasome activity declined, along with increased expression of the anti-inflammatory Alpha7 nicotinic acetylcholine receptor (α7nAChR) and the inhibition of TLR4/NF-κB signaling. Consequently, high doses of nicotine also reduced ASC expression, caspase-1 activity and IL-1β secretion in macrophages. Collectively, these results suggest a dual regulatory function of nicotine on NLRP3 inflammasome activation in macrophages, that is involved with the pro-inflammatory effects of lysosomal destabilization and ROS production. We also show nicotine mediates anti-inflammatory effects by activating α7nAChR at high doses.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"61-74"},"PeriodicalIF":4.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140876284","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}

{"title":"Sodium Crotonate Alleviates Diabetic Kidney Disease Partially Via the Histone Crotonylation Pathway.","authors":"Yanqiu He, Yumei Xie, Tingting Zhou, Dongze Li, Xi Cheng, Ping Yang, Changfang Luo, Yijun Liu, Man Guo, Qin Wan, Pijun Yan, Chenlin Gao, Yuan-Yuan Zhang, Xiao-Dong Sun, Yong Xu, Wei Huang","doi":"10.1007/s10753-024-02047-w","DOIUrl":"10.1007/s10753-024-02047-w","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is a common microvascular complication of diabetes, inflammation and fibrosis play an important role in its progression. Histone lysine crotonylation (Kcr) was first identified as a new type of post-translational modification in 2011. In recent years, prominent progress has been made in the study of sodium crotonate (NaCr) and histone Kcr in kidney diseases. However, the effects of NaCr and NaCr-induced Kcr on DKD remain unclear. In this study, db/db mice and high glucose-induced human tubular epithelial cells (HK-2) were used respectively, and exogenous NaCr and crotonoyl-coenzyme A (Cr-CoA) as intervention reagents, histone Kcr and DKD-related indicators were detected. The results confirmed that NaCr had an antidiabetic effect and decreased blood glucose and serum lipid levels and alleviated renal function and DKD-related inflammatory and fibrotic damage. NaCr also induced histone Kcr and histone H3K18 crotonylation (H3K18cr). However, NaCr and Cr-CoA-induced histone Kcr and protective effects were reversed by inhibiting the activity of Acyl-CoA synthetase short-chain family member 2 (ACSS2) or histone acyltransferase P300 in vitro. In summary, our data reveal that NaCr may mitigate DKD via an antidiabetic effect as well as through ACSS2 and P300-induced histone Kcr, suggesting that Kcr may be the potential molecular mechanism and prevention target of DKD.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":"254-275"},"PeriodicalIF":4.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186196","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}