Molecular and Cellular Biochemistry最新文献

{"title":"Dilated cardiomyopathy: from genes and molecules to potential treatments.","authors":"Xiumei Wang, Zekun Lang, Zeyi Yan, Jing Xu, Jinyuan Zhang, Lianhang Jiao, Haijun Zhang","doi":"10.1007/s11010-025-05269-0","DOIUrl":"https://doi.org/10.1007/s11010-025-05269-0","url":null,"abstract":"<p><p>Dilated cardiomyopathy is a myocardial condition marked by the enlargement of the heart's ventricular chambers and the gradual decline in systolic function, frequently resulting in congestive heart failure. Dilated cardiomyopathy has obvious familial characteristics, and mutations in related pathogenic genes can account for about 50% of patients with dilated cardiomyopathy. The most common genes related to dilated cardiomyopathy include TTN, LMNA, MYH7, etc. With more and more research on these genes, it will undoubtedly provide more potential targets and therapeutic pathways for the treatment of dilated cardiomyopathy. In addition, myocardial inflammation, myocardial metabolism abnormalities and cardiomyocyte apoptosis all have an important impact on the pathogenesis of dilated cardiomyopathy. Approximately half of sudden deaths among children and adolescents, along with the majority of patients undergoing heart transplantation, stem from cardiomyopathy. Therefore, precise and prompt clinical diagnosis holds paramount importance. Currently, diagnosis primarily hinges on the patient's medical background and imaging tests, with the significance of genetic testing steadily gaining prominence. The primary treatment for dilated cardiomyopathy remains heart transplantation. However, the scarcity of donors and the risk of severe immune rejection underscore the pressing need for novel therapies. Presently, research is actively exploring preclinical treatments like stem cell therapy as potential solutions.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143743277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis: a potential therapeutic target in cardio-cerebrovascular diseases.","authors":"Chenlong Jiang, Yang Yan, Tianlin Long, Jiawei Xu, Cuicui Chang, Meili Kang, Xuanqi Wang, Yuhua Chen, Junlin Qiu","doi":"10.1007/s11010-025-05262-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05262-7","url":null,"abstract":"<p><p>Cardio-cerebrovascular diseases (CCVDs) are the leading cause of global mortality, yet effective treatment options remain limited. Ferroptosis, a novel form of regulated cell death, has emerged as a critical player in various CCVDs, including atherosclerosis, myocardial infarction, ischemia-reperfusion injury, cardiomyopathy, and ischemic/hemorrhagic strokes. This review highlights the core mechanisms of ferroptosis, its pathological implications in CCVDs, and the therapeutic potential of targeting this process. Additionally, it explores the role of Chinese herbal medicines (CHMs) in mitigating ferroptosis, offering novel therapeutic strategies for CCVDs management. Ferroptosis is regulated by several key pathways. The GPX4-GSH-System Xc- axis is central to ferroptosis execution, involving GPX4 using GSH to neutralize lipid peroxides, with system Xc- being crucial for GSH synthesis. The NAD(P)H/FSP1/CoQ10 axis involves FSP1 regenerating CoQ10 via NAD(P)H, inhibiting lipid peroxidation independently of GPX4. Lipid peroxidation, driven by PUFAs and enzymes like ACSL4 and LPCAT3, and iron metabolism, regulated by proteins like TfR1 and ferritin, are also crucial for ferroptosis. Inhibiting ferroptosis shows promise in managing CCVDs. In atherosclerosis, ferroptosis inhibitors reduce iron accumulation and lipid peroxidation. In myocardial infarction, inhibitors protect cardiomyocytes by preserving GPX4 and SLC7A11 levels. In ischemia-reperfusion injury, targeting ferroptosis reduces myocardial and cerebral damage. In diabetic cardiomyopathy, Nrf2 activators alleviate oxidative stress and iron metabolism irregularities. CHMs offer natural compounds that mitigate ferroptosis. They possess antioxidant properties, chelate iron, and modulate signaling pathways like Nrf2 and AMPK. For example, Salvia miltiorrhiza and Astragalus membranaceus reduce oxidative stress, while some CHMs chelate iron, reducing its availability for ferroptosis. In conclusion, ferroptosis plays a pivotal role in CCVDs, and targeting it offers novel therapeutic avenues. CHMs show promise in reducing ferroptosis and improving patient outcomes. Future research should explore combination therapies and further elucidate the molecular interactions in ferroptosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peripheral nerves-cancer cross-talk: the next frontier in cancer treatment.","authors":"Leihan Wang, Teng Qi, Lingyun Tang, Yuehan Wang, Zhenni ChenLiu, Daorong Wang, Dong Tang","doi":"10.1007/s11010-025-05256-5","DOIUrl":"https://doi.org/10.1007/s11010-025-05256-5","url":null,"abstract":"<p><p>The nervous system, which regulates organogenesis, homeostasis, and plasticity of the organism during human growth and development, integrates physiological functions of all organ systems, including the immune system. Its extensive network of branches throughout the body reaches the tumor microenvironment (TME), where it secretes neurotransmitters that directly regulate or influence immune cells. This, in turn, indirectly affects the occurrence, development, and metastasis of cancer. Conversely, cancer cells are now understood to secrete neurotrophic factors that remodel the nervous system. Targeting the cross-talk between the nervous system and cancer represents a promising strategy for cancer treatment, some aspects of which have been confirmed in clinical trials. This review addresses gaps in our understanding of the interaction between peripheral nerves and various human cancers. At the intersection of neuroscience and cancer biology, new targets for neuroscience-based cancer therapies are emerging, establishing a significant new pillar in cancer treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Molecular and biochemical evidence on the protective role of ellagic acid and silybin against oxidative stress-induced cellular aging.","authors":"Maryam Baeeri, Solmaz Mohammadi-Nejad, Mahban Rahimifard, Mona Navaei-Nigjeh, Shermineh Moeini-Nodeh, Reza Khorasani, Mohammad Abdollahi","doi":"10.1007/s11010-025-05266-3","DOIUrl":"https://doi.org/10.1007/s11010-025-05266-3","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between herpesviruses and alzheimer's disease: a meta-analysis based on case-control studies.","authors":"Huilin Feng, Kexiao Pan, Zulfa Ismail Shabani, Hongju Wang, Wenqiang Wei","doi":"10.1007/s11010-025-05263-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05263-6","url":null,"abstract":"<p><p>Herpesviruses infection has been found to be implicated in the etiology of Alzheimer's disease (AD). However, the results remain controversial. This systematic meta-analysis was aimed to evaluate the relationship between Herpesviruses infection and the risk of developing AD. Relevant literature was searched from five databases, including CNKI, PubMed, Web of Science, Embase, and Cochrane Library, to obtain case-control studies (published between the date of database establishment and February 2025; no language restrictions) that compared the Herpesviruses positivity in AD patients and healthy controls. Among all existing studies, there are more abundant published case-control studies on the relationship between HSV-1, HCMV and Alzheimer's disease. Therefore, we chose these two viruses to further explore their association with Alzheimer's disease. The quality of the included studies was evaluated by the NOS scale. The Review Manager 5.3 software was used to calculate the odds ratio (OR) and 95% confidence interval (95% CI) for meta-analysis. Publication bias was investigated using the funnel plots, Begg's and Egger's publication bias plots. Twenty-one eligible studies were included to investigate the association between HSV-1 and AD. The results of the meta-analysis indicated that HSV-1 infection is a risk factor for AD (OR = 1.39, 95% CI = (1.14-1.69), P < 0.05)). In the subgroup analysis, the pooled ORs of HSV-1 infection associated with AD were 1.28 (95% CI: 0.74-2.22) in literature prior to 2010;1.44 (95% CI: 1.14-1.82) in literature after 2010; 1.27(95% CI: 1.01-1.60) in studies from Europe; 1.22(95% CI: 0.66-2.27) in studies from North America;1.89 (95% CI: 1.19-3.02) in studies from Asia; 1.38 (95% CI: 1.10-1.74) in the clinical diagnosis group; 1.52 (95% CI: 0.84-2.74) in the autopsy group. The pooled OR of APOE4 positivity and AD risk was 5.51 (95% CI: 4.33-7.01). The association between HCMV and AD was analyzed in seven studies. The pooled result showed that HCMV infection is not a risk factor for AD (OR = 0.83, 95% CI = 0.63-1.09). Our latest meta-analysis suggests that HSV-1 infection is a risk factor for the risk of AD. Therefore, anti-HSV-1 infection can serve as a potential therapeutic strategy for control of AD incidence. There is insufficient evidence to support association between HCMV and AD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adiponectin mediated metabolic and sphingolipid alterations in preventing endothelial dysfunction.","authors":"Vinnyfred Vincent, Himani Thakkar, Atanu Sen, Ashutosh Bansal, Ujjalkumar Subhash Das, Abishek Gunasekaran, Neerja Bhatla, Thirumurthy Velpandian, Archna Singh","doi":"10.1007/s11010-025-05268-1","DOIUrl":"https://doi.org/10.1007/s11010-025-05268-1","url":null,"abstract":"<p><p>Endothelial dysfunction is an early indicator of atherosclerosis. Adiponectin, a hormone secreted by adipose tissue with insulin-sensitizing and anti-inflammatory properties, offers protection against atherosclerosis. This study investigated the metabolic and sphingolipid alterations in endothelial cells linked to the protective effects of adiponectin against endothelial dysfunction. Human Umbilical Endothelial Cells (HUVECs) were treated with Tumor Necrosis Factor-alpha (TNF-α) to induce endothelial dysfunction. AdipoRon and SKI-I were used to study the effects of adiponectin and sphingosine kinase inhibition in HUVECs. Metabolic changes and sphingolipid alterations were assessed to understand changes in lipid metabolism, and RNA sequencing was used to quantify the transcriptomics changes. TNF-α treatment significantly upregulated glycolysis and downregulated long-chain fatty acid oxidation and mitochondrial ATP production, while AdipoRon co-treatment partially reversed these metabolic effects. In HUVECs, TNF-α treatment increased intracellular C16 and C18 ceramides and Sphingosine 1-Phosphate (S1P) while decreasing extracellular S1P. AdipoRon Co-treatment reversed these effects; AdipoRon also reversed the transcriptional changes induced by TNF-α. Sphingosine kinase inhibition in HUVECs led to mitochondrial dysfunction at the metabolic and transcriptional levels. This study provides insights into potential therapeutic strategies targeting endothelial metabolism while unraveling a novel mitochondrial modulation mediated by sphingosine kinases in endothelial cells.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clonal hematopoiesis of indeterminate potential: contribution to disease and promising interventions.","authors":"Chongjie Li, Chunxiang Zhang, Xiuying Li","doi":"10.1007/s11010-025-05261-8","DOIUrl":"https://doi.org/10.1007/s11010-025-05261-8","url":null,"abstract":"<p><p>In clonal hematopoiesis of indeterminate potential (CHIP), subpopulations of blood cells carrying somatic mutations expand as the individual ages, and this expansion may elevate risk of blood cancers as well as cardiovascular disease. Individuals at higher risk of CHIP and therefore of CHIP-associated disease can be identified through mutational profiling, and the apparently central role of inflammation in CHIP-associated disease has emerged as a potential therapeutic target. While CHIP is often associated with negative health outcomes, emerging evidence suggests that some CHIP-related mutations may also exert beneficial effects, indicating a more complex role in human health. This review examines current understanding of the epidemiology and clinical significance of CHIP and the role of inflammation in driving its association with disease risk. It explores the mechanisms linking CHIP to inflammation and risk of cardiovascular and other diseases, as well as the potential of personalizing therapies against those diseases for individuals with CHIP.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of microRNAs in cardiorenal syndrome.","authors":"Yilin Ren, Hui Lin, Junnan Guo, Xiaole Su, Lihua Wang, Xi Qiao","doi":"10.1007/s11010-025-05253-8","DOIUrl":"https://doi.org/10.1007/s11010-025-05253-8","url":null,"abstract":"<p><p>Cardiac and kidney diseases are intimately linked through numerous pathophysiological pathways, frequently exerting reciprocal influences on one another. This interconnection often culminates in heightened morbidity and mortality rates within the clinical spectrum of cardiorenal syndrome (CRS). CRS is categorized into five types based on the primary organ involved and the chronicity of the condition. Each type of CRS encompasses a complex array of pathophysiological mechanisms. In recent years, the field of microRNAs (miRNAs) has risen to prominence, playing a crucial role in the pathogenesis of a multitude of diseases. By uncovering novel therapeutic targets through the study of miRNAs that influence the expression of the CRS genes, the prognostic outcomes for patients could be significantly improved. This article provides a comprehensive review, examining the pathophysiological underpinnings of CRS, miRNAs alterations and their associated mechanisms in various forms of CRS, as well as the potential of miRNAs in precision medicine and the use of miRNAs for the diagnosis of the disease.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"14-3-3ζ: an optimal housekeeping protein for western blot analysis in swine rotator cuff tendon studies.","authors":"Resmi Rajalekshmi, Vikrant Rai, Devendra K Agrawal","doi":"10.1007/s11010-025-05255-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05255-6","url":null,"abstract":"<p><p>Healthy biomechanics of the shoulder involving rotator cuff muscles and rotator cuff tendon (RCT) is pivotal for joint stability, yet co-morbid conditions like hyperlipidemia and hyperglycemia can lead to degenerative changes jeopardizing tendon integrity. A change in protein expression, the functional moiety for molecular events, may result in altered healing of RCT and prolonged morbidity. Expression and activity of proteins are critical while investigating the underlying molecular and cellular changes involved in tendinopathy. While investigating the changes in the protein expression of various inflammatory mediators, we observed that the Western Blot bands for commonly used housekeeping genes (GAPDH, β-actin, and α-tubulin) were not uniform in different tendon samples. Therefore, we investigated for an optimal housekeeping gene for Western blot analysis in swine RCT under normal and hyperlipidemic conditions, as this is essential for accurate normalization of protein expression. The study evaluated several housekeeping genes-GAPDH, beta-actin, alpha and beta-tubulin, Ubiquitin C, Cyclophilin A, TATA-box binding protein, and 14-3-3ζ-to ensure robust normalization across experimental setups. The results revealed that the protein expression of 14-3-3ζ was uniform in all samples, thereby validating its suitability as a stable housekeeping protein. The findings are important while studying the RCT pathology in a clinically relevant animal model, like swine, which mimics human RCT and provides translationally significant findings. Thus, the 14-3-3ζ protein will be an ideal housekeeping gene in the design of experiments utilizing musculoskeletal tissues.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone H2A: a promising diagnostic marker in heart failure with reduced versus preserved ejection fraction.","authors":"Desislava K Tsoneva, Diana Buzova, Salvatore Daniele Bianco, Antoniya Kisheva, Mesut Rushid, Tanya Ivanova, Yoto Yotov, Jan Cerveny, Tommaso Mazza, Manlio Vinciguerra","doi":"10.1007/s11010-025-05254-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05254-7","url":null,"abstract":"<p><p>The diagnosis of heart failure with preserved left ventricle ejection fraction (HFpEF) remains a challenge, with score-based algorithms showing varying diagnostic performance and biomarkers sometimes inconclusive. This study aimed to examine whether circulating histones and histone complexes, which recently emerged as robust biomarkers of inflammation and stroke, show distinct profiles in plasma from healthy individuals, HF with reduced EF (HFrEF), and HFpEF patients. We evaluated the plasma histone profile of 30 sex/age-matched healthy individuals, 22 HFpEF and 25 HFrEF prior any therapeutic intervention. ImageStreamX-based detection approach was used to measure the levels of circulating particles positive for core histones H2A, H2B, H3, H4, histone variants macroH2A1.1 and macroH2A1.2. While we found increased levels of most of the histones and histone complexes in both HFpEF and HFrEF patients, H2A was significantly elevated only in HFpEF, compared to healthy individuals (p-value = 0.002) and to HFrEF (p-value = 0.00008). In line with these findings, H2A showed positive correlation with EF (r = 0.493). We identified a plasma histone profile able to detect HF and differentiate between HFpEF and HFrEF using a high throughput and imaging flow cytometry-adapted liquid biopsy.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}