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galectin-3 as a Prognostic Biomarker of Left Ventricular Assist Device Implantation Outcomes

ASAIO JOURNAL 2025年第2期71卷 136-142页

作者： Hoang, Ryan Acosta, Mary E. Belkin, Mark N. Rasheed, Nabeel F. Siddiqi, Umar Cruz, Jennifer M. Lupo, Sydney E. Stonebraker, Corinne R. Kalantari, Sara Grinstein, Jonathan Univ Chicago Dept Surg Sect Cardiac Surg Chicago IL USA Univ Chicago Dept Cardiol Sect Adv Heart Failure 5841 S MarylandRm E-500 Chicago IL 60637 USA

We assessed the prognostic potential of galectin-3 in a sample of 159 heart failure patients who received a left ventricular assist device (LVAD) implant from 2012 to 2020. Clinical outcomes included hemodynamic data, right heart failure (RHF), hemocompatibility-related adverse events (HRAEs), and mortality. galectin-3 was compounded into Michigan-RVF and EUROMACS-RHF risk scores and compared to the noncompounded risk scores. Right heart failure was significantly correlated with galectin (p = 0.004) on a continuous spectrum. Inotrope duration was significantly correlated to galectin-3 (interquartile range [IQR]: 7.58-8.65, p < 0.001) along with INTERMACS score (IQR: 2.14-1.90, p < 0.001). Intensive care unit length of stay (median 8 days, p = 0.02), blood urea nitrogen (p < 0.001), creatinine (p < 0.001), and pulmonary artery pulsatility index (p = 0.05) were also significantly correlated with galectin-3. In our c-statistic analysis, the predictive value for RHF improved when galectin-3 was included for both the Michigan-RVF (0.80-0.86) and EUROMACS-RHF (0.77-0.82) risk scores. When elevated over a binary cutoff of 18.2 ng/ml, galectin-3 significantly correlated with HRAEs (p = 0.014) and mortality (p = 0.031). galectin-3 shows great promise as a predictive biomarker in patients implanted with durable LVADs. In addition to significant correlation with key clinical outcomes, galectin-3 enhanced the Michigan-RVF and EUROMACS-RHF risk scores in predicting progression to RHF.

关键词： left ventricular assist device galectin-3 Biomarker RHF Michigan-RVF

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galectin-3 activates microglia and promotes neurological impairment via NLRP3/pyroptosis pathway following traumatic brain injury

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BRAIN RESEARCH 2025年 1855卷 149560-149560页

作者： Sun, Yan Gao, Sheng-Qing Wang, Xue Li, Tao Han, Yan-Ling Miao, Shu-Hao Zhao, Ran Zheng, Xiao-Bo Qiu, Jia-Yin Jin, Wang-Xuan Gao, Chao-Chao Zhou, Meng-Liang Nanjing Med Univ Jinling Hosp Jinling Sch Clin Med Dept Neurosurg Nanjing Peoples R China Nanjing Univ Nanjing Jinling Hosp Affiliated Hosp Med SchDept Neurosurg Nanjing Peoples R China Nanjing Univ Chinese Med Jinling Clin Med Coll Nanjing Peoples R China

Background: Externally caused traumatic brain injury (TBI) poses a woeful worldwide health concern, bringing about disability, death, and prolonged neurological impairment. Increased galectin-3 levels have been linked to unfavorable outcomes in several neurological conditions. This study explores the role of galectin-3 in TBI, specifically examining its contribution to neuroinflammation. Methods: BV2 microglia cells treated with lipopolysaccharide (LPS) and a mouse model of TBI were applied to investigate the impact of galectin-3 on neuroinflammation following TBI. Western blotting and immunofluorescence labeling were applied for evaluating protein levels and colocalization. Adeno-associated virus (AAV) that targets microglia was used to knock down galectin-3 in microglia. Nissl staining and the modified neurologic severity score were employed in evaluating neural survival and neurological function, and the cognitive impairment following TBI was assessed by the Y-Maze and Morri water maze test. Results: galectin-3 expression was shown to rise dramatically after TBI, peaking between days five and seven. In vitro, BV2 cells treated with LPS showed reduced NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation when galectin-3 was inhibited. In LPS-activated microglia, galectin-3 inhibition specifically decreased the expression of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-kappa B), p-NF-kappa B, NLRP3, Apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, and Gasdermin D (GSDMD). Injection with AAV containing siRNA to knock down galectin-3 in microglia was operated on mice in vivo. Following TBI, this knockdown led to reduced NLRP3 inflammasome activation, neuronal death, neurological impairments and cognitive impairment. Conclusions: Our foundings indicate that modulating microglia-derived galectin-3 following TBI to reduce neuroinflammation could serve as a promising therapeutic strategy.

关键词： galectin-3 NLRP3 inflammasome Traumatic brain injury Microglia Neuroinflammation

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M2-polarized tumor-associated macrophage-secreted exosomal lncRNA NEAT1 upregulates galectin-3 by recruiting KLF5 and promotes HCC immune escape

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JOURNAL OF CELL COMMUNICATION AND SIGNALING 2025年第1期19卷 e12060页

作者： Yuan, Wei Sun, Qigang Zhu, Xiaodan Li, Bo Zou, Yongping Liu, Zhehao Hainan Med Univ Hainan Gen Hosp Dept Emergency Surg Hainan Affiliated Hosp 19 Xiuhua Rd Haikou 570311 Hainan Peoples R China Hainan Med Coll Hainan Gen Hosp Hainan Hosp Dept Hepatobiliary & Pancreat Surg Haikou Peoples R China

HCC cell immune escape is a critical element in the evolution of HCC malignancy. Herein, the regulatory mechanism of lncRNA NEAT1 in regulating HCC immune escape was investigated. Exosomes were isolated from M2 TAMs using ExoQuick-TC. Then, HCC cells were incubated with M2 TAMs-derived exosomes (M2-exos). The activation of perforin+CD8+ T cells was measured using flow cytometry. The secretion of IFN-gamma was assessed using ELISA. Cell viability and migration were detected using CCK8 and Transwell assays, respectively. RIP and RNA pull-down assays were used to investigate the link between NEAT1 and KLF5. ChIP and dual-luciferase reporter assays were used to investigate the interaction between KLF5 and the LGALS3 promoter. Our results showed that NEAT1, KLF5 and galectin-3 were overexpressed in HCC tissues. M2-exos treatment promoted HCC proliferation, migration, and immune escape. It was found that NEAT1 was enriched in M2-TAMs and M2-exos. M2-exos facilitated HCC immune escape, whereas NEAT1 silencing reversed this effect. NEAT1 upregulated galectin-3 in HCC cells by recruiting KLF5. Mechanically, M2-TAM-derived exosomal NEAT1 induced HCC immune escape by upregulating KLF5/galectin-3 axis. M2-TAM-derived exosomal NEAT1 upregulated galectin-3 in HCC cells by recruiting KLF5 to promote perforin+CD8+ T cell depletion and further accelerate HCC immune escape.

关键词： exosomes galectin-3 hepatocellular carcinoma immune escape KLF5 NEAT1 tumor-associated macrophages

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galectin-1 and galectin-3 in male reproduction - impact in health and disease

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SEMINARS IN IMMUNOPATHOLOGY 2025年第1期47卷 1-10页

作者： Fijak, Monika Hasan, Hiba Meinhardt, Andreas Justus Liebig Univ Giessen Inst Anat & Cell Biol Hessian Ctr Reprod Med Aulweg 123 D-35392 Giessen Germany

The formation and differentiation of mature, motile male germ cells, which can fertilize the egg and ensure successful implantation and development of a healthy embryo, are essential functions of the testis and epididymis. Spermatogenesis is a complex, multistep process that results in the formation of motile haploid gametes, requiring an immunoregulatory environment to maintain tolerance to developing neo-antigens. Different cell types (Sertoli cells, macrophages), immunoregulatory factors and tolerance mechanisms are involved. In this context, possible effects of galectins on the immunoregulatory functions and fertilization ability of male germ cells are postulated. galectins are pleiotropic lectins involved in the homeostasis, modulation of immune responses and pathological processes. Despite the well-recognized role of galectins in female reproduction, the functions of galectins in the male reproductive organs, particularly the testis and epididymis, remain largely unexplored. Among the galectins, galectin-1 and galectin-3 are the best-studied in these organs. This review summarizes the current knowledge of the cellular expression and the roles of galectin-1 and galectin-3 in testis and epididymis and discusses their functions in spermatogenesis, steroidogenesis, epididymal maturation of spermatozoa and inflammatory response.

关键词： galectin-1 galectin-3 Testis Epididymis Immune privilege

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galectin-3 in metabolic disorders: mechanisms and therapeutic potential

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Trends in Molecular Medicine 2025年第5期31卷 424-437页

作者： Jiang, Qian Zhao, Qijin Li, Pingping State Key Laboratory of Bioactive Substance and Function of Natural Medicines Institute of Materia Medica Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100050 China Diabetes Research Center of Chinese Academy of Medical Sciences Beijing 100050 China CAMS Key Laboratory of Molecular Mechanism and Target Discovery of Metabolic Disorder and Tumorigenesis Beijing 100050 China

galectin-3 (Gal3), a β-galactoside-binding lectin, is expressed predominantly in immunological and inflammatory cells. Gal3 expression is elevated in metabolic diseases, including obesity, diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD), and plays an important role in the progression of these diseases. In this review, we summarize the structure and post-translational modifications of Gal3 and the cellular functions of Gal3 according to its subcellular localization. We focused on the pathological functions and molecular mechanisms of Gal3 in various cell types. In particular, extracellular Gal3 and intracellular Gal3 may have different physiological and pathological functions. We also discuss promising Gal3 inhibitors or antibodies that are currently in clinical trials and outstanding questions and challenges for future pursuit. © 2024 Elsevier Ltd

关键词： galectin-3 mechanisms metabolic disorders therapeutic potential

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Effects of Troxerutin on Oxidative Stress, Inflammation and galectin-3 Expression in Intracerebroventricular Kainic Acid-Induced Neurotoxicity

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INFLAMMATION 2025年 1-15页

作者： Demir, Mehmet Elbe, Hulya Cetinavci, Dilan Saruhan, Ercan Karabuk Univ Fac Med Dept Physiol Karabuk Turkiye Mugla Sitki Kocman Univ Fac Med Dept Histol & Embryol Mugla Turkiye Mugla Training & Res Hosp Dept Histol & Embryol Mugla Turkiye Mugla Sitki Kocman Univ Fac Med Dept Med Biochem Mugla Turkiye

Excitotoxicity caused by excessive concentration of the excitatory neurotransmitter glutamate causes neuronal cell death and promotes neurodegenerative disorders. The neuroexcitant neurotoxin kainic acid (KA) induces excitotoxicity, leading to neuronal death via oxidative stress and inflammation, and its experimental use is widespread. This study was designed to determine the protective effect of Troxerutin (TXR) and its relationship with galectin-3 (Gal-3) in experimental excitotoxicity with neuroinflammation and oxidative stress. Fifty male Wistar rats were divided into five groups (n = 10): Control group rats received intraperitoneal (ip) normal saline for 6 days. Sham group rats received a single dose of intracerebroventricular (icv) normal saline on the first day. KA group rats were treated with a single dose of KA;icv-0.5 mu g/mu l). TXR group rats treated with TXR for 6 days: ip-100 mg/kg) and KA + TXR group rats treated with KA (single dose) and TXR (6 days). It was observed that malondialdehyde (MDA) and interleukin-1 beta (IL-1 beta) levels increased and reduced glutathione (GSH) levels decreased in the cerebral cortex of rats with KA neurotoxicity. TXR treatment caused a significant improvement in MDA and GSH levels and a significant decrease in IL-1 beta levels in rats with the excitotoxicity model. Gal-3 expressions in the hippocampus and cerebellum increased in KA-treated rats, whereas TXR treatment decreased Gal-3 expressions. In addition, histopathological changes caused by KA administration showed improvement in TXR-treated groups. In conclusion, the findings showed that TXR treatment attenuated KA-induced neurotoxicity by reducing oxidative tissue damage, inflammatory response and Gal-3 expression.

关键词： Troxerutin Intracerebroventricular Kainic acid Oxidative stress Inflammation galectin-3

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An elevated level of soluble suppression of tumorigenicity 2, but not galectin-3, is associated with the presence of coronary artery disease in hypertensive patients

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HYPERTENSION RESEARCH 2025年第2期48卷 650-661页

作者： Miura-Takahashi, Erika Tsudome, Riku Suematsu, Yasunori Tachibana, Tetsuro Kato, Yuta Kuwano, Takashi Sugihara, Makoto Tashiro, Kokei Shiga, Yuhei Kamimura, Hidetoshi Miura, Shin-ichiro Fukuoka Univ Hosp Dept Pharm Fukuoka Japan Fukuoka Univ Sch Med Dept Cardiol Fukuoka Japan

We investigated whether there were associations between coronary artery disease (CAD) and soluble suppression of tumorigenicity (sST2) and galectin-3 levels at the time of coronary artery computed tomography angiography (CCTA) for CAD screening. The subjects consisted of 429 patients who underwent CCTA examination. CAD was diagnosed when there was 50% or more stenosis in the coronary artery. Patient backgrounds were collected and plasma levels of sST2 and galectin-3 were measured. The presence or absence of CAD and factors that contributed to CAD were analyzed for all patients and for those with or without hypertension (HTN). The CAD group had significantly higher sST2 levels than the non-CAD group, whereas there was no significant difference in galectin-3 levels. The number of patients in the non-HTN and HTN groups was 174 and 255, respectively. In the HTN group, the CAD group was significantly older than the non-CAD group and had higher sST2 levels. Multivariate analysis showed that the factors that contributed to CAD in the HTN group were age and sST2 levels. On the other hand, in the non-HTN group, the CAD group was significantly older than the non-CAD group, and had a higher proportion of males and higher sST2 levels, while the contributing factors for the CAD group were age and male gender, but not sST2. In conclusion, a higher level of sST2, but not galectin-3, was a contributing factor for CAD in HTN patients. However, in non-HTN patients, a high level of sST2 was not a contributing factor for CAD.

关键词： Coronary artery computed tomography angiography Soluble suppression of tumorigenicity 2 galectin-3 Coronary artery disease

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Development and validation of galectin-3 and CVAI-based model for predicting cognitive impairment in type 2 diabetes

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JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION 2025年第4期48卷 1017-1031页

作者： Zhou, Xueling Dai, Ning Yu, Dandan Niu, Tong Wang, Shaohua Southeast Univ Sch Med Nanjing Peoples R China Southeast Univ Dept Endocrinol Affiliated Zhongda Hosp Nanjing Peoples R China Maanshan Peoples Hosp Dept ENT Maanshan Peoples R China

ObjectiveThe objective of this study is to develop a predictive model combining multiple indicators to quantify the risk of mild cognitive impairment (MCI) in T2DM *** study included Chinese T2DM patients who were hospitalized at Zhongda Hospital between November 2021 and May 2023. Clinical data, including demographics, medical history, biochemical tests, and cognitive status, were collected. Cognitive assessment was performed using neuropsychological tests, and MCI was diagnosed based on the Montreal Cognitive Assessment (MoCA) scores. The dataset was randomly divided into a training set and a validation set in a 7:3 ratio. Logistic regression analysis was conducted to identify factors influencing MCI in the training set. A nomogram-based scoring model was then developed by integrating these findings with high-risk clinical variables, and its performance was validated in the validation *** this study, T2DM patients were divided into a training set and a validation set in a 7:3 ratio. There were no significant differences in MCI incidence, demographics, or clinical characteristics between the two groups, confirming the appropriateness of model construction. In the training set, galectin-3 and CVAI were significantly negatively correlated with cognitive function (MoCA and MMSE scores), and this negative correlation remained after adjusting for confounding variables. Logistic regression analysis revealed that age, CVAI, and galectin-3 significantly increased the risk of MCI, while years of education had a protective effect. The constructed nomogram model, which integrated age, sex, education level, hypertension, CVAI, and galectin-3 levels, exhibited high predictive performance (C-index of 0.816), with AUCs of 0.816 in the training set and 0.858 in the validation set, outperforming single indicators. PR curve analysis further validated the superiority of the nomogram *** straightforward, highly accurate, and interactive nomog

关键词： Mild cognitive impairment Type 2 diabetes galectin-3 CVAI Nomogram

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Protective effect of galectin-3 inhibitor against cardiac remodelling in an isoprenaline-induced myocardial infarction in type 2 diabetes

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ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY 2025年第1期131卷 94-107页

作者： Mahmoud, Manal Moustafa Hassan, Mai Mohammed Elsayed, Hany El-Sebaee Fares, Amal E. Saber, Mona M. Rashed, Laila Ahmed Abdelwahed, Omaima Mohammed Cairo Univ Fac Med Dept Med Physiol Cairo Egypt Cairo Univ Fac Med Dept Histol & Cell Biol Cairo Egypt Cairo Univ Fac Pharm Dept Pharmacol & Toxicol Cairo Egypt Cairo Univ Fac Med Dept Med Biochem Cairo Egypt

Type 2 Diabetes mellitus (T2DM) has the potential to impair cardiac function and cause heart failure. We aimed to study the cardioprotective influence of Galactin-3 (Gal-3) inhibitor;modified citrus pectin (MCP) in isoprenaline induced myocardial infarction (MI) in T2DM rats. Forty rats were allocated into 4 groups;groups I and II served as control. T2DM was provoked in groups III and IV by serving them high fat diet followed by a single low dose of Streptozotocin (STZ), then group IV were administered MCP in drinking water for 6 weeks. Groups III and IV were then subcutaneously injected isoprenaline hydrochloride once daily on the last 2 successive days to induce MI. MCP restored echocardiographic parameters with significant decline in Gal-3 area % in cardiac tissue alongside protection against cardiac remodelling. our data showed that there is a protective potential for Gal-3 inhibitor (MCP) against cardiac injury in isoprenaline induced MI in T2DM.

关键词： Type 2 DM myocardial infarction galectin-3 modified citrus pectin

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Discovery of Galactopyranose-1-carboxamides as a New Class of Small, Novel, Potent, Selective, and Orally Active galectin-3 Inhibitors

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CHEMMEDCHEM 2025年第0期 e202401012页

作者： Zumbrunn, Cornelia Remen, Lubos Sager, Christoph P. Grisostomi, Corinna Stamm, Christina Krusi, Daniela Glutz, Sven Schmidt, Gunther Nayler, Oliver Iglarz, Marc Mac Sweeney, Aengus Chambovey, Alain Mueller, Manon Mueller, Celia Bourquin, Geoffroy Meyer, Solange Huhn, Eva Cattaneo, Christophe Vercauteren, Magali Gatfield, John Bolli, Martin H. Idorsia Pharmaceut Ltd Hegenheimermattweg 91 CH-4123 Allschwil Switzerland

galectin-3 (Gal-3), a beta-galactoside-binding lectin, is implicated in diverse cellular functions ranging from immune response modulation to tissue homeostasis. Notably, increased Gal-3 expression has been linked to the progression of numerous diseases, including cancer, fibrosis, and cardiovascular disorders, underscoring its potential as a therapeutic target. Small molecule inhibitors have been discovered and are valuable tools to study such diseases. We report here the discovery of novel, galactose-based, small molecule inhibitors such as compound 12 which are orally bioavailable and show efficacy in a mouse model of acute liver injury and fibrosis (CCl4 model). The use of structure-based drug design (docking of a virtual library of amides based on acid 2) was key in the process towards potent, nanomolar inhibitors.

关键词： cancer fibrosis galectin-3 inflammation inhibitor

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