Sai Praneeth Chaparala, Abhishek Hanumanpratap Singh Kshatri, Amritha Suresh, Akkshaya Suresh Kumar, Akshitha Talasila, Thaimye Joseph, Swathi Lenin Babu Naraginiti
{"title":"Personalized antiplatelet therapy: are we ready for a precision medicine approach.","authors":"Sai Praneeth Chaparala, Abhishek Hanumanpratap Singh Kshatri, Amritha Suresh, Akkshaya Suresh Kumar, Akshitha Talasila, Thaimye Joseph, Swathi Lenin Babu Naraginiti","doi":"10.1515/jbcpp-2025-0139","DOIUrl":"https://doi.org/10.1515/jbcpp-2025-0139","url":null,"abstract":"<p><p>Dual antiplatelet therapy (DAPT), combining aspirin with a P2Y<sub>12</sub> inhibitor, remains central to secondary prevention after acute coronary syndrome and percutaneous coronary intervention. However, substantial interindividual variability in antiplatelet response, particularly clopidogrel resistance associated with CYP2C19 polymorphisms, has challenged the conventional \"one-size-fits-all\" approach and increased interest in precision-guided antiplatelet strategies. This narrative review synthesized literature identified through PubMed, Scopus, Web of Science, and Google Scholar, focusing on randomized trials, genotype-guided studies, platelet function testing (PFT), meta-analyses, guideline statements, and emerging artificial intelligence (AI)-based prediction models. Evidence suggests that genotype-guided therapy, PFT-guided treatment, and individualized DAPT duration may improve the balance between ischemic protection and bleeding risk in selected high-risk populations. However, routine implementation remains limited by inconsistent clinical outcome benefits, heterogeneous testing strategies, modest risk-score performance, cost, infrastructure barriers, and variable guideline recommendations. Precision-guided DAPT is promising, but broader adoption requires stronger prospective evidence, standardized testing pathways, and real-world validation.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Laila A Damiati, Mohammed A Baghdadi, Safa A Damiati, Raghad Alrasheed, Alaa Alrasheed, Ayad Turky, Samar Damiati
{"title":"Predicting COVID-19 severity using machine learning: the role of clinical parameters, blood groups, and vaccination status across age groups.","authors":"Laila A Damiati, Mohammed A Baghdadi, Safa A Damiati, Raghad Alrasheed, Alaa Alrasheed, Ayad Turky, Samar Damiati","doi":"10.1515/jbcpp-2026-0123","DOIUrl":"10.1515/jbcpp-2026-0123","url":null,"abstract":"<p><strong>Objectives: </strong>COVID-19 has had strong impacts on both global health systems and economies. Therefore, understanding disease severity and progression is crucial. This cross-sectional study aims to investigate possible link between clinical factors, laboratory parameters, and age on COVID-19 severity. Machine-learning (ML) methods were used to analyze a dataset to explore the relationships between these variables and disease progression.</p><p><strong>Methods: </strong>In this study, 177 hospitalized COVID-19 patients were divided into five age groups. A range of biomarkers, including hematological parameters, electrolytes, and liver and renal function tests, were analyzed. Several parameters had acceptable sensitivity and specificity and indicated cut-off levels between patient age groups. Furthermore, ML was used to find an interaction between blood group, pneumococcal vaccine status, and COVID-19 symptoms to explore potential relationships.</p><p><strong>Results: </strong>The main findings were that various biomarkers were differentially regulated in COVID-19 patients across different age groups. Furthermore, the interpretation of the obtained results indicated a significant association between the presence of symptoms during the course of the illness and pneumococcal vaccination status. Additionally, feature selection analysis employing machine learning techniques, specifically Random Forest and Mutual Information, identified the most important features within the analyzed dataset.</p><p><strong>Conclusions: </strong>Although blood group and Pneumococcal vaccine showed weak influence on the presence of COVID-19 symptoms, our findings shed light on the relative importance of the most influencing predictors on COVID-19 severity, which may provide valuable-insights for better risk assessment.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"325-336"},"PeriodicalIF":0.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Olufemi I Oluranti, Lawrence D Adedayo, Esther O Ojo-Ayangoke, Kolawole O Adio, Olamide F Aluko, Michelle D Orefuwa, Ifeoluwa D Oladejo, Praise O Toye, Omobolanle E Ayantoyinbo, Babatunde A Alabi
{"title":"Ferulic acid and not ascorbic acid reversed cardiac energy metabolism disruption in acute aluminum chloride exposed mice via PPARα/AMPK pathway.","authors":"Olufemi I Oluranti, Lawrence D Adedayo, Esther O Ojo-Ayangoke, Kolawole O Adio, Olamide F Aluko, Michelle D Orefuwa, Ifeoluwa D Oladejo, Praise O Toye, Omobolanle E Ayantoyinbo, Babatunde A Alabi","doi":"10.1515/jbcpp-2026-0031","DOIUrl":"10.1515/jbcpp-2026-0031","url":null,"abstract":"<p><strong>Objectives: </strong>Proper cardiac function depends on adequate supply and metabolism of energy substrates. Aluminum chloride exposure has been linked to adverse cardiac events. This study investigated the ameliorative effect of ferulic acid and ascorbic acid in dysregulated cardiac energy metabolism in aluminum chloride-exposed mice.</p><p><strong>Methods: </strong>Thirty mice were randomized into five groups (n=6): control (0.1 % distilled water), aluminum chloride (AlCl<sub>3</sub>, 100 mg/kg, <i>p.o</i>), aluminum chloride and ferulic acid (AlCl<sub>3</sub>, 100 mg/kg; FA<sub>20</sub>, 10 mg/kg, <i>p.o</i>), aluminum chloride and ferulic acid (AlCl<sub>3</sub>, 100 mg/kg; FA<sub>10</sub>, 10 mg/kg, <i>p.o</i>), aluminum chloride and ascorbic acid (AlCl<sub>3</sub>, 100 mg/kg; Vit. C, 100 mg/kg), daily for 7 days. Cardiac metabolic enzymes activities were analyzed spectrophotometrically; substrate transporters and regulators of energy metabolism were analyzed using immunohistochemistry.</p><p><strong>Results: </strong>AlCl<sub>3</sub> increased hexokinase activity and reduced pyruvate-dehydrogenase activity compared with the control. AlCl<sub>3</sub> significantly reduced the expression of glucose transporter-4 (GLUT 4), carnitine palmitoyl-transferase 1β (CPT1β), peroxisome proliferator-activated receptor-alpha (PPARα) and AMP-activated protein kinase (AMPK) compared with the control. However, FA reversed the effect of AlCl<sub>3</sub> by significantly increasing hexokinase and pyruvate dehydrogenase activities, increasing the expression of GLUT4, CPT1β, PPARα and AMPK.</p><p><strong>Conclusions: </strong>FA mitigate against cardiac metabolic disruption caused by acute exposure to AlCl<sub>3</sub> through PPARα and AMPK modulation.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"425-435"},"PeriodicalIF":0.0,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gestational diabetes mellitus and long-term cancer risk: a narrative review of epidemiological and mechanistic evidence.","authors":"Ana Lúcia Abdo Ladeira","doi":"10.1515/jbcpp-2026-0136","DOIUrl":"10.1515/jbcpp-2026-0136","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy and is increasingly recognized as a marker of long-term metabolic vulnerability. Beyond its established association with cardiometabolic diseases, emerging epidemiological evidence suggests a potential link between GDM and increased cancer risk, particularly hormone-sensitive malignancies such as endometrial and breast cancer. This narrative review integrates epidemiological and mechanistic evidence exploring the relationship between GDM and long-term oncological susceptibility. Hyperglycemia, hyperinsulinemia, and chronic low-grade inflammation associated with GDM may contribute to proliferative signaling and metabolic dysregulation. Among the proposed mechanisms, insulin/IGF-1 signaling represents one of the most biologically plausible links, whereas pathways involving PI3K/Akt/mTOR activation, metabolic reprogramming, and tumor microenvironment alterations remain largely inferred from broader oncological literature. In addition, persistent metabolic stress during pregnancy may induce long-term epigenetic and immunometabolic changes potentially associated with carcinogenic susceptibility. Although current evidence does not establish a direct causal relationship between GDM and cancer, the integration of epidemiological and mechanistic findings supports the hypothesis that GDM may function as an early marker of systemic metabolic vulnerability associated with increased long-term oncological risk. Further longitudinal and mechanistic studies are needed to clarify this relationship and its clinical implications.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"381-386"},"PeriodicalIF":0.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"GDF-11 triggers cold-induced browning and metabolic activation of adipose tissue.","authors":"Serena Sagliocchi, Lucia Acampora, Caterina Miro, Annarita Nappi, Federica Restolfer, Monica Dentice, Annunziata Gaetana Cicatiello","doi":"10.1515/jbcpp-2026-0087","DOIUrl":"10.1515/jbcpp-2026-0087","url":null,"abstract":"<p><strong>Objectives: </strong>White adipose tissue (WAT) browning enhances energy expenditure and represents a promising target for metabolic disease. Growth differentiation factor 11 (GDF-11), a circulating member of the TGF-β superfamily, has been implicated in metabolic regulation, but its role in adipose tissue plasticity remains unclear. This study investigated whether GDF-11 regulates WAT browning and the underlying mechanisms.</p><p><strong>Methods: </strong>Mice were exposed to cold to induce browning, and GDF-11 expression and SMAD2/3 activation were assessed in brown adipose tissue (BAT), visceral and subcutaneous WAT, and skeletal muscle. We combined <i>in vivo</i> results to <i>in vitro</i> approaches, 3T3-L1 cells were differentiated into white or brown adipocytes and treated with recombinant GDF-11 to evaluate gene expression and cellular phenotype.</p><p><strong>Results: </strong>Cold exposure increased GDF-11 expression and activated SMAD2/3 signaling, particularly in BAT and subcutaneous WAT. This was associated with upregulation of thermogenic and metabolic genes, including <i>Ucp1</i>, <i>Ucp3</i>, <i>Dio2</i>, and <i>PGC-1α</i>. <i>In vitro</i>, GDF-11 enhanced thermogenic and adipogenic gene expression and induced morphological features consistent with browning. GDF-11 also increased <i>SmyD1</i> expression, supporting a role in metabolic activation.</p><p><strong>Conclusions: </strong>GDF-11 promotes adipose tissue thermogenic remodeling through SMAD2/3 signaling and may represent a potential therapeutic target for metabolic diseases.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"395-407"},"PeriodicalIF":0.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148258198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Environmental diabetogens: biochemical links between microplastic exposure, endocrine disruption, and glucose metabolic dysfunction.","authors":"Robin Singh, Jaspreet Kaur, Bhumika Upadhyay","doi":"10.1515/jbcpp-2026-0068","DOIUrl":"10.1515/jbcpp-2026-0068","url":null,"abstract":"<p><p>The increase in the incidence of type 2 diabetes mellitus (T2DM) worldwide cannot be attributed solely to genetic and lifestyle factors, underscoring the growing role of environmental metabolic disruptors. Microplastics are increasingly being identified as potential environmental diabetogens, owing to the high risk of human exposure and the potential of microplastics to act as EDC carriers. This review aims to integrate the biochemical and molecular evidence for the association between microplastic exposure and the development of impaired glucose metabolism via endocrine, inflammatory, and metabolic signaling pathways. These microplastics and additives, such as bisphenols, phthalates, and POPs, interact with nuclear hormone receptors, including the estrogen receptor, peroxisome proliferator-activated receptor, and aryl hydrocarbon receptor, resulting in aberrant transcriptional control of genes involved in the regulation of metabolism. Microplastics exposure may cause oxidative stress-mediated activation of stress kinases, inhibition of insulin receptor substrate-1, suppression of PI3K-Akt signaling, GLUT4 translocation, and mitochondrial dysfunction, which together result in systemic insulin resistance. In addition, β-cell damage, systemic inflammation, and changes in the gut microbiome interfere with the regulation of glucose metabolism in the liver, muscle, and adipose tissues.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"267-279"},"PeriodicalIF":0.0,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148258246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neurophysiology of abdominal pain: a review of peripheral, spinal, central mechanisms and emerging research trends.","authors":"Ravindran Revand, Rani Kumari","doi":"10.1515/jbcpp-2026-0034","DOIUrl":"10.1515/jbcpp-2026-0034","url":null,"abstract":"<p><p>Experience of visceral pain occurs when there is discomfort originating from internal organs of the body, often resulting from injury, infection, inflammation, ischemia, tumors, or neuropathy. In clinical practice, visceral pain is recognized as one of the most prevalent and incapacitating types of pain. It encompasses a diverse range of conditions impacting organs within thoracic, pelvic, and abdominal regions. Specifically, visceral pain of abdominal origin often presents as diffuse and poorly defined sensations of varying intensities. This characteristic arises from relatively sparse sensory innervation of visceral organs and divergent nature of visceral inputs. In addition, visceral noxious stimuli differ significantly from somatic pain triggers. Perception of visceral noxious stimuli from abdominal organs starts with transduction of signals at peripheral processes of sensory neurons, and transmission of these impulses to cortical centers, processing pain. Pathways concerned with nociceptive signaling from abdomen include intricate meshwork of neurons interconnecting different functional loci within nervous system. This review brings together current concepts on how abdominal pain is processed at several interconnected levels. Understanding of physiological pathways involved in abdominal pain processing supplemented with history, physical examinations, necessary biochemical, histopathological and radiological investigations constitute the cornerstone for abdominal pain management in clinical settings.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"281-292"},"PeriodicalIF":0.0,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Serum bilirubin as a predictor of complicated appendicitis: a diagnostic accuracy study.","authors":"Edwin Joy, Thesneem Changanath Kader","doi":"10.1515/jbcpp-2026-0023","DOIUrl":"10.1515/jbcpp-2026-0023","url":null,"abstract":"<p><strong>Objectives: </strong>Early identification of complicated acute appendicitis remains a clinical challenge. Serum bilirubin has been proposed as a potential biomarker reflecting disease severity rather than primary diagnosis. To evaluate the diagnostic accuracy of serum bilirubin in predicting complicated acute appendicitis using histopathology as the reference standard.</p><p><strong>Methods: </strong>A cross-sectional diagnostic accuracy study was conducted among 150 adult patients undergoing appendectomy for suspected acute appendicitis at a tertiary care center. Preoperative serum bilirubin levels were recorded. Histopathological examination served as the gold standard. Diagnostic performance indices, including sensitivity, specificity, predictive values, accuracy, and receiver operating characteristic (ROC) analysis, were calculated.</p><p><strong>Results: </strong>Acute appendicitis was confirmed by histopathology in 82.7 % of cases, of which 11.3 % were complicated. Elevated serum bilirubin (≥1.2 mg/dL) was observed in 71.4 % of complicated appendicitis cases compared to 26.4 % of non-complicated cases (p=0.001). For predicting complicated appendicitis, serum bilirubin demonstrated a sensitivity of 71.4 %, specificity of 73.6 %, and a high negative predictive value of 95.3 %. ROC analysis yielded an AUC of 0.712, indicating fair diagnostic accuracy, with an optimal cut-off of 1.15 mg/dL.</p><p><strong>Conclusions: </strong>Serum bilirubin is a valuable adjunctive biomarker for predicting complicated appendicitis and effectively ruling out severe disease when levels are normal. Its integration into preoperative assessment may aid risk stratification and clinical decision-making.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"409-415"},"PeriodicalIF":0.0,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"New insight on hepatic encephalopathy: a comprehensive review.","authors":"Ahmed A Sedik, Renad Alrefaei","doi":"10.1515/jbcpp-2025-0166","DOIUrl":"10.1515/jbcpp-2025-0166","url":null,"abstract":"<p><p>Hepatic encephalopathy (HE) encompasses a wide spectrum of neuropsychiatric disturbances that arise as a consequence of acute or chronic liver dysfunction. It represents a critical event in the natural history of cirrhosis and serves as an independent predictor of morbidity and mortality in affected patients worldwide. The clinical manifestations of HE range from subtle cognitive impairments, such as poor concentration, memory deficits, anxiety, depression, and insomnia, to severe psychomotor abnormalities, disorientation, and coma. Hyperammonemia is widely regarded as the central hallmark of HE pathogenesis and remains a cornerstone in both diagnosis and therapeutic monitoring. However, elevated ammonia levels do not always correlate with clinical severity, and some patients may present with significant neurological impairment despite near-normal ammonia concentrations. This discrepancy highlights the multifactorial mechanisms underlying HE, including neuroinflammation, oxidative stress, alterations in neurotransmission, and gut-liver-brain axis dysregulation. In this review, we provide a comprehensive overview of the pathogenesis, clinical spectrum, diagnostic approaches, and current as well as emerging therapeutic strategies for hepatic encephalopathy, with a focus on recent advances that may improve patient outcomes.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"293-303"},"PeriodicalIF":0.0,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Peng He, Wei Tan, Yanjie Zhu, Jing Fan, Wang Liu, Liya Huang, Yu Liu, Guangbo Tan
{"title":"Ginsenoside Rg1 attenuates right ventricular remodeling in hypoxic pulmonary hypertension and is associated with suppression of HIF-1α-related glycolytic signaling.","authors":"Peng He, Wei Tan, Yanjie Zhu, Jing Fan, Wang Liu, Liya Huang, Yu Liu, Guangbo Tan","doi":"10.1515/jbcpp-2026-0090","DOIUrl":"10.1515/jbcpp-2026-0090","url":null,"abstract":"<p><strong>Objectives: </strong>To determine whether ginsenoside Rg1 attenuates right ventricular remodeling in hypoxic pulmonary hypertension and whether this effect is associated with suppression of HIF-1α-related glycolytic signaling.</p><p><strong>Methods: </strong>Male C57BL/6 mice were exposed to normobaric hypoxia (10 % O<sub>2</sub>) for 4 weeks and assigned to control, model, sildenafil, Rg1, or HIF-1α knockdown groups (n=10 per group). Pulmonary function, hemodynamic parameters, right ventricular hypertrophy, histopathology, oxidative stress, apoptosis, immunofluorescence, and protein expression in right ventricular tissue were evaluated.</p><p><strong>Results: </strong>Hypoxia reduced forced expiratory volume in 0.3 s/forced vital capacity and increased mean pulmonary arterial pressure, right ventricular systolic pressure, and right ventricular hypertrophy index. It also induced myocardial disorganization, collagen deposition, oxidative stress, apoptosis, and increased expression of HIF-1α, glucose transporter 1, hexokinase 2, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3, lactate dehydrogenase A, transforming growth factor beta 1, Smad2, and collagen I. Rg1 significantly attenuated these abnormalities, with a pattern broadly comparable to HIF-1α knockdown.</p><p><strong>Conclusions: </strong>Rg1 attenuated hypoxia-induced right ventricular remodeling and fibrosis and was associated with reduced oxidative injury, apoptosis, and HIF-1α-related glycolytic and profibrotic signaling.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"437-446"},"PeriodicalIF":0.0,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}