{"title":"Research advance in mesenchymal stem cell-based therapy for diabetic nephropathy.","authors":"Yan Hui, Yuyang Dong, Yi Liu","doi":"10.1080/13813455.2024.2447532","DOIUrl":"https://doi.org/10.1080/13813455.2024.2447532","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is the main cause of end-stage kidney disease and has become a global public health problem. Currently, treatment of DN is limited to alleviating disease progression rather than curing diseases or restoring renal function, thus more effective therapeutic strategies against DN are urgently needed. Mesenchymal stem cells (MSCs) have been widely applied in the prevention and treatment of DN. Preclinical studies have proved that MSCs exhibited favourable therapeutic effects on DN by regulation of hyperglycaemia, reduction of urinary albumin, and protecting renal function. Hence this review provides an overview of the biological properties of MSCs, summarises the regulatory mechanisms of MSC-based therapy for DN, presents ongoing or completed clinical trials, as well as discusses the potential challenges and new strategies of MSCs in the treatment of DN, with the aim of providing a balanced and unbiased view of MSC transplantation as promising therapeutic strategies for DN.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":"131 3","pages":"379-392"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elissa Kerli Fernandes, Patrick Türck, Cristina Campos Carraro, Silvio Tasca, Isabel Cristina Teixeira Proença, Victor De Mello Palma, Fernanda Visioli, Iraci Lucena Da Silva Torres, Adriane Belló-Klein, Alexandre Luz De Castro, Alex Sander Da Rosa Araujo
{"title":"Boldine reduces left ventricle oxidative stress in isoproterenol-induced adrenergic overload experimental model.","authors":"Elissa Kerli Fernandes, Patrick Türck, Cristina Campos Carraro, Silvio Tasca, Isabel Cristina Teixeira Proença, Victor De Mello Palma, Fernanda Visioli, Iraci Lucena Da Silva Torres, Adriane Belló-Klein, Alexandre Luz De Castro, Alex Sander Da Rosa Araujo","doi":"10.1080/13813455.2024.2441363","DOIUrl":"10.1080/13813455.2024.2441363","url":null,"abstract":"<p><p>Sustained adrenergic overload in the heart causes maladaptive cardiac remodelling, which involves oxidative stress. Boldine (BOL) has antioxidant activity and represents a novel therapeutic approach. This study explored the cardioprotective role of BOL in adverse left ventricular remodelling induced by isoproterenol. The rats were divided into four groups: control; BOL (25 mg/kg daily); isoproterenol (ISO) (5 mg/kg daily), and ISO + BOL. Morphometric, echocardiographic, and oxidative stress parameters were evaluated. BOL attenuated both cardiac hypertrophy and increased diastolic volume caused by adrenergic overstimulation (P < 0.05). BOL treatment reduced lipid peroxidation induced by ISO (ISO vs. ISO + BOL; P < 0.05), and this effect was associated with increased superoxide dismutase (SOD) (ISO vs. ISO + BOL; P < 0.05) and glutathione-S-transferase levels (GST) (ISO vs. ISO + BOL; P < 0.05). This data suggest that BOL may improve cardiac oxidative stress and attenuate some parameters of adverse cardiac remodelling.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"445-454"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Evaluation of the clinical significance of BTG1 gene expression and pepsinogen in serum and cancerous tissue and gastric atrophy.","authors":"Yousef Paridar, Homa Hosseinpour, Maysam Mard-Soltani, Somayeh Pouria Mehr, Neda Shakerian, Davood Alinezhad Dezfuli, Saeed Khalili, Mohammad Reza Abyaz","doi":"10.1080/13813455.2025.2458560","DOIUrl":"10.1080/13813455.2025.2458560","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to assess the expression changes of BTG1, PGI, and PGII in tissues and serum of patients with gastric cancer, atrophic gastritis, and healthy individuals.</p><p><strong>Methods: </strong>QRT-PCR was used to measure BTG1, PGI, and PGII expression in 30 cancers, 30 atrophic gastritis, and 30 healthy tissue samples. Serum levels of PGI and PGII were measured using ELISA. Statistical tests included the Mann-Whitney U and independent T-test. Covariates like tumour stage and <i>H. pylori</i> status were considered.</p><p><strong>Results: </strong>BTG1 expression was significantly lower in cancer and gastritis tissues. Serum PGI and PGII levels were significantly reduced in cancer patients (<i>P</i> ≤ 0.001).</p><p><strong>Discussion: </strong>The PGI/PGII ratio in serum emerged as a strong non-invasive biomarker for distinguishing cancer from healthy individuals. While BTG1 provides insights into gastric carcinogenesis, its clinical utility is limited due to the need for tissue samples. The serum-based PGI/PGII ratio shows greater promise as a non-invasive screening tool for GC.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"503-512"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Silvio Tasca, Patrick Türck, Daniela Drosdowski, Cristina Campos Carraro, Adriane Belló-Klein, Alexandre Luz De Castro, Alex Sander Da Rosa Araujo
{"title":"Melatonin improves adverse vascular remodelling and redox homeostasis in monocrotaline-induced pulmonary arterial hypertension.","authors":"Silvio Tasca, Patrick Türck, Daniela Drosdowski, Cristina Campos Carraro, Adriane Belló-Klein, Alexandre Luz De Castro, Alex Sander Da Rosa Araujo","doi":"10.1080/13813455.2024.2446822","DOIUrl":"10.1080/13813455.2024.2446822","url":null,"abstract":"<p><p>This study explored the effects of melatonin on cardiac and vascular function, and redox homeostasis in model PAH. Male Wistar rats were divided into: control (CTR), monocrotaline [MCT (60 mg/kg, single dose i.p)], monocrotaline + sildenafil [MCT + SIL (50 mg/kg/day)], and monocrotaline + melatonin [MCT + MEL (10 mg/kg/day)]. This protocol lasted 21 days. Echocardiographic, morphometric, histological, vascular reactivity, and oxidative/nitrosative stress analyses were performed. The reduced diastolic function and AT/ET ratio in the MCT group were partially attenuated by melatonin and sildenafil treatment (<i>p</i> < 0.05). Increased RV hypertrophy and pulmonary congestion were reduced by both treatments (<i>p</i> < 0.05). MCT-induced pulmonary arteriolar muscle layer hypertrophy was also reduced by both treatments (<i>p</i> < 0.05). MCT and MCT + SIL present diminished vasorelaxation as compared to control (<i>p</i> < 0.05). Augmented oxidative/nitrosative stress and reduced glutathione-s-transferase activity in MCT were mitigated by both treatments (<i>p</i> < 0.05). Then, melatonin was as effective as sildenafil against PAH-induced oxidative stress and pathological vascular remodelling.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"455-466"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Christine Skagen, Stanislava Stevanovic, Hege Gilbø Bakke, Tuula A Nyman, Maria Stensland, Eili Tranheim Kase, Olga Horakova, Arild C Rustan, G Hege Thoresen
{"title":"Reduced lipid and glucose oxidation and reduced lipid synthesis in AMPKα2<sup>-/-</sup> myotubes.","authors":"Christine Skagen, Stanislava Stevanovic, Hege Gilbø Bakke, Tuula A Nyman, Maria Stensland, Eili Tranheim Kase, Olga Horakova, Arild C Rustan, G Hege Thoresen","doi":"10.1080/13813455.2024.2449409","DOIUrl":"10.1080/13813455.2024.2449409","url":null,"abstract":"<p><p>Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) plays a crucial role in regulation of metabolic homeostasis. To understand the role of the catalytic α2 subunit of AMPK in skeletal muscle energy metabolism, myotube cultures were established from <i>AMPKα2<sup>+/+</sup></i> and <i>AMPKα2<sup>-/-</sup></i> mice. Myotubes from <i>AMPKα2<sup>-/-</sup></i> mice had lower basal oleic acid and glucose oxidation compared to myotubes from <i>AMPKα2<sup>+/+</sup></i> mice. However, the relative response to mitochondrial uncoupling was increased for oleic acid oxidation. Incorporation of acetate into lipids was also lower in myotubes from <i>AMPKα2<sup>-/-</sup></i> mice. Proteomics analysis revealed that <i>AMPKα2<sup>-/-</sup></i> myotubes had upregulated pathways related to mitochondrial function and fatty acid oxidation, and decreased pathways related to fatty acid biosynthesis. In conclusion, ablation of AMPKα2 catalytic subunit in skeletal muscle cells resulted in reduced basal oxidation of glucose and fatty acids, however upregulated pathways related to mitochondrial function and fatty acid oxidation and reduced lipid formation.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"483-492"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tumour protein p53-activated lncRNA PGM5-AS1 suppresses lung cancer growth and stemness by targeting R-spondin1 <i>via</i> microRNA-1247-5p.","authors":"Peng Yang, Hong Gu, Xuanqin Wu, Geng Chen, Heng Liu, Zhongliang Chen","doi":"10.1080/13813455.2025.2459318","DOIUrl":"10.1080/13813455.2025.2459318","url":null,"abstract":"<p><strong>Objective: </strong>This study was to investigated the inhibitory role of the tumour protein p53 (TP53)-activated PGM5-AS1 in lung cancer (LC) cell proliferation, invasion, and CSC-like properties and its underlying mechanisms.</p><p><strong>Methods: </strong>The effect of PGM5-AS1 on LC cell development was determined. Stem cell markers, aldehyde dehydrogenase activity in cells were tested, as well as the ability of stem cells to form spheroids. The interaction of PGM5-AS1 and TP53 was determined. The binding link of PGM5-AS1, miR-1247-5p, and R-spondin1 (RSPO1) was verified.</p><p><strong>Results: </strong>PGM5-AS1 was elevated by a combination of TP53 and PGM5-AS1 promoters. PGM5-AS1 was a molecular sponge of miR-1247-5p in LC cells, and miR-1247-5p targeted RSPO1. Elevating PGM5-AS1 or repressing miR-1247-5p restrained LC cell growth and stemness, which were reversed by depression of RSPO1.</p><p><strong>Conclusion: </strong>This study conveys that TP53-elevated PGM5-AS1 mediates miR-1247-5p to target RSPO1, thereby inhibiting LC growth and stemness, representing a novel avenue for LC therapy.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"513-525"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"AMPK activation; a potential strategy to mitigate TKI-induced cardiovascular toxicity.","authors":"Nasser Safaie, Gholamreza Idari, Diba Ghasemi, Mobasher Hajiabbasi, Vahid Alivirdiloo, Shahab Masoumi, Mahdi Zavvar, Ziba Majidi, Yousef Faridvand","doi":"10.1080/13813455.2024.2426494","DOIUrl":"10.1080/13813455.2024.2426494","url":null,"abstract":"<p><p>The introduction of Tyrosine Kinase Inhibitors (TKIs) has revolutionised cancer treatment, yet concerns regarding cardiovascular toxicity have surfaced. This piece delves into the interplay between AMP-activated protein kinase (AMPK) signalling and TKI-induced cardiovascular toxicity. The study unravels the intricate relationship between AMPK activation and TKI-induced cardiovascular toxicity, aiming to ascertain whether AMPK can play a strategic role in mitigating adverse effects. Beyond unravelling mechanistic insights, the research sets the stage for future therapeutic approaches, envisioning AMPK activation as a pivotal connection for balancing effective cancer treatment with cardiovascular well-being. As research advances, the potential of AMPK activation not only addresses challenges in TKI-induced cardiovascular toxicity but also shapes the future landscape of personalised anticancer therapies. The article explores the mechanisms of TKI-induced toxicity, AMPK's impact on cardiovascular health, and the potential therapeutic implications of AMPK activation in alleviating TKI-associated toxicities.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"329-341"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wanyi Chen, Jin Chen, Ziqiong Cheng, Weilun Chen, Huiping Zhang
{"title":"Lipophagy: exploring its association with male reproductive system disorders and investigating potential mechanisms.","authors":"Wanyi Chen, Jin Chen, Ziqiong Cheng, Weilun Chen, Huiping Zhang","doi":"10.1080/13813455.2024.2446840","DOIUrl":"10.1080/13813455.2024.2446840","url":null,"abstract":"<p><strong>Background: </strong>Lipid metabolism, one of the three major metabolic processes, plays a crucial role in male fertility, particularly when lipid homeostasis is disrupted. Lipid droplets (LDs), cellular organelles that store lipids primarily in the form of triglycerides and cholesterol esters, serve as central hubs in lipid metabolism.The degradation of LDs is regulated by lipases and lipophagy.</p><p><strong>Objective:: </strong>This review explores the various forms of lipophagy, its molecular mechanisms, and its critical role in male fertility. Specifically, it examines the association between lipophagy and male infertility, sexual dysfunction, and reproductive cancers.</p><p><strong>Methods:: </strong>This review synthesizes current research on the molecular pathways regulating lipophagy, focusing on its impact on male reproductive health.</p><p><strong>Results:: </strong>Lipophagy is essential for maintaining lipid homeostasis in male reproductive tissues. Dysfunction of lipophagy is associated with impaired sperm function, infertility, sexual dysfunction, and an increased risk of reproductive cancers in men.</p><p><strong>Conclusion:: </strong>Lipophagy plays a pivotal role in regulating lipid metabolism and maintaining male fertility. It may serve as a potential therapeutic target for treating male reproductive disorders.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"366-378"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ayman S Soliman, Amira A Abdelfattah, Osama M Ahmed, Safy S Gaber
{"title":"Lepidine potentiates the antidiabetic effect of metformin in nicotinamide/streptozotocin-induced diabetic male rats.","authors":"Ayman S Soliman, Amira A Abdelfattah, Osama M Ahmed, Safy S Gaber","doi":"10.1080/13813455.2025.2459865","DOIUrl":"10.1080/13813455.2025.2459865","url":null,"abstract":"<p><p>Metformin is used as a first-line treatment of type 2 diabetes mellitus (T2DM) and is effective as monotherapy and in combination with other glucose-lowering medications. Lepidine, a natural product found in <i>Lepidium sativum</i>, had antidiabetic, antioxidant, anticancer, anti-inflammatory, and hypolipidemic effects. This study aimed to assess the effects of lepidine alone and in combination with metformin in nicotinamide (NA)/streptozotocin (STZ)-induced diabetic Wistar rats. T2DM was induced by intraperitoneal injection of NA 15 minutes before intraperitoneal injection of STZ. Diabetic rats were orally treated with lepidine (20 mg/kg body weight) and/or metformin (70 mg/kg body weight) every other day for four weeks. Both lepidine and metformin treated diabetic rats showed a significant decrease in fasting blood glucose (FBG), amelioration of serum lipid profile, increase in serum insulin, and C-peptide , and downregulation in the elevated serum tumour necrosis α (TNF-α) level in association with the improvement in the pancreatic islet integrity and function. In conclusion, the lepidine has potent anti-diabetic effects and may add more to the therapeutic value of metformin when the two agents are used in combination. However, further clinical studies on human beings with T2DM are required to assess the efficacy and safety of the combination of metformin and lepidine before its approval and therapeutic application.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"526-538"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Siska Andrina Kusumastuti, Dwi Aris Agung Nugrahaningsih, Mae Sri Hartati Wahyuningsih
{"title":"Metformin attenuates inflammation and improves insulin sensitivity in coculture of LPS-induced 3T3-L1 adipocytes and RAW 264.7 macrophages mediated by IRS-1/GLUT-4 pathway.","authors":"Siska Andrina Kusumastuti, Dwi Aris Agung Nugrahaningsih, Mae Sri Hartati Wahyuningsih","doi":"10.1080/13813455.2025.2460102","DOIUrl":"10.1080/13813455.2025.2460102","url":null,"abstract":"<p><strong>Objective: </strong>Metformin is an anti-diabetic drug used to control blood glucose levels. The effects of metformin on insulin sensitivity in inflammation-induced adipocytes are not fully understood.This study aimed to explore the mechanism of metformin on insulin sensitivity enhancement in the coculture of LPS-induced 3T3-L1 adipocytes and RAW 264.7 macrophages.</p><p><strong>Material and methods: </strong>Insulin resistance was induced in coculture cells using Lipopolysaccharide, followed by adding 25, 50, and 100 µg/ml of metformin for 24 h of incubation. Glucose consumption, GLUT-4, IRS-1, and IL-6 mRNA expressions were quantified.</p><p><strong>Results: </strong>Metformin, starting at a concentration of 25 µg/ml, enhanced glucose consumption, upregulated GLUT-4 mRNA expression, and stimulated the expression of IRS-1 mRNA in coculture cells at 100 µg/ml of concentration. Additionally, Metformin inhibited inflammation by reducing IL-6 mRNA expression in coculture cells up to 100 µg/ml.</p><p><strong>Discussion and conclusion: </strong>These findings suggest that metformin attenuated inflammation and improved insulin sensitivity in inflammation-induced adipocytes that may be mediated by the IRS-1/GLUT-4 pathway.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"549-555"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}