Molecular and Cellular Biomedical Sciences最新文献

{"title":"Molecular Adaptation of Cardiac Remodeling in Metabolic Syndrome: Focus on AMPK, SIRT1 and PGC-1a","authors":"Andika Yusuf Ramadhan, Vivian Soetikno","doi":"10.21705/mcbs.v8i1.367","DOIUrl":"https://doi.org/10.21705/mcbs.v8i1.367","url":null,"abstract":"Obesity, lack of physical activity, and genetic predisposition might play a pivotal role in pathogenesis of metabolic syndrome. Cardiac function alteration including hemodynamic changes, contractility function, arrhythmia, and cellular respiratory function, might happen due to chronic condition in metabolic syndrome. Insulin resistance, neurohormonal activation and chronic inflammation might contribute to these changes. Cardiomyocyte had capabilities to adapt from these abnormalities, one of them is the activation of cellular pathway to resist cardiac injury from metabolic syndrome. This molecular pathway involves three proteins, including AMP-activated protein kinase (AMPK), sirtuin-1 (SIRT1) and peroxisome proliferator-activated receptor γ coactivator-α (PGC-1α). The aim of this narrative review is to elucidate role of AMPK, SIRT1, and PGC-1α in cardiac adaptation against cardiac dysfunction in metabolic syndrome. AMPK, SIRT-1, and PGC-1α contribute to adapt and to repair the cardiac injury resulting from celullar and mechanical stress from metabolic syndrome and prevent cardiac remodeling event. Several pathological events, such as insulin resistance, induce alteration of switching energy fuel to the heart, causing cardiomyocte to rely on glucose metabolism and lipotoxicity, leading to damages of cardiomyocyte through reactive oxygen species (ROS) generation and lipid peroxidation. Increase of ROS promotes cardiac injury followed by necrotic and apoptotic events. AMPK, SIRT1, and PGC-1α act as cardioprotector molecule against metabolic syndrome insults to several mechanism such as: AMPK play role as counter act of lipotoxicity and insulin resistance through increasing insulin sensitivity and regulate redox reaction. SIRT1 plays role in regulating apoptotic genes and PGC-1α repairs cardiac fuel sources. Activation of AMPK/SIRT1/PGC-1α prevent cardiac remodeling due to metabolic syndrome by increasing insulin sensitivity, increases mitochondrial biogenesis and reduce pro-apoptotic signals in cardiomyocte.Keywords: AMPK/SIRT1/PGC-α, cardiac remodeling, metabolic syndrome","PeriodicalId":514464,"journal":{"name":"Molecular and Cellular Biomedical Sciences","volume":" 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140387553","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":"Percutaneous Secundum Atrial Septal Defect Closure: Failure Rate and Procedural Predictors","authors":"Elien Yuwono, Eka Gunawijaya, Y. P. V. K. Ni","doi":"10.21705/mcbs.v8i1.442","DOIUrl":"https://doi.org/10.21705/mcbs.v8i1.442","url":null,"abstract":"Background: Percutaneous atrial septal defect (ASD) closure is one of therapeutic options for patients with a suitable ASD anatomy, however in developing countries, the exact figure and procedural characteristics remain unknown. Therefore, this study was conducted to identify the failure rate and procedural predictors of the percutaneous ASD closure.Materials and methods: A retrospective study using a database of all patients undergoing percutaneous ASD closure was conducted between March 2010 to November 2023. Patients who developed a pulmonary hypertensive crisis during the procedure were excluded. Procedural and echocardiographic parameter were measured and analyzed.Results: A total of 112 samples were included in this study, 74.1% were female and 55.36% were pediatric patients. The failure rate was 12.5% (n=14) with diameter index was higher in the failed group. Unpaired T-test revealed that ASD size was one of the predictor failure in pediatric patients (mean diameter: 24.7±6.46 mm vs. 16.36±5.94 mm, p=0.001). There were no statistically significant variations in rim diameters, while compared with all patients with appropriate rims (rim ≥7mm), the failure rate was higher in patients with two rims measuring between 5.9 and 6.9 mm and rims less than 5 mm. Two patients presented with device embolization and required surgical device removal.Conclusion: The failure rate of percutaneous ASD closure was 12.5%. A larger ASD increases the risk of failure of percutaneous closure in pediatric patients. Furthermore, patient with 5-6.9 mm on two or more rims as well as those with rim less than 5 mm, have a higher failure rate.Keywords: secundum atrial septal defect, percutaneous closure, failure rate","PeriodicalId":514464,"journal":{"name":"Molecular and Cellular Biomedical Sciences","volume":" 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140387282","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":"Application of Omics and Bioinformatics Technologies in Response to COVID-19 Pandemic","authors":"Abebe M. Aga, A. A. Woldesemayat","doi":"10.21705/mcbs.v8i1.363","DOIUrl":"https://doi.org/10.21705/mcbs.v8i1.363","url":null,"abstract":"The medical biotechnology community has undertaken significant endeavors to gain a comprehensive understanding of SARS-CoV-2’s biology and pathogenesis mechanisms. Omics approaches and technologies have been widely employed in the fight against SARS-CoV-2. Since the onset of the virus outbreak, researchers have demonstrated how recent omics and bioinformatics technological advancements have contributed to the diagnosis, vaccine development, treatment, and control of disease transmission. Studies conducted since the outbreak have been collected and summarized, with a focus on bioinformatics approaches and their contribution to controlling this pandemic. Developments and advanced omics technology in connection to the COVID-19 pandemic have been analyzed. The multi-omics technology, which offers various strategies in identifying potential diagnostics, therapeutics, studies of variants of concern, and drug repurposing approaches, has been assessed. Pandemic response has seen the application of multi-omics and pan-genomics approaches, including genomics, metabolomics, transcriptomics, proteomics, epigenomics, clustered regularly interspaced short palindromic repeats (CRISPR) technology, host-pathogen interactions, artificial intelligence, and machine learning in various research areas. Additionally, bioinformatics and mathematical modeling have played a significant role in disease control. The use of smart technologies to control virus transmission and predict patients’ health conditions and treatment outcomes has also been crucial. Transcriptome analysis has emerged as a major application, contributing to the generation of new knowledge on viral sequences and intracellular signaling pathways that regulate viral infection and pathogenesis mechanisms. The sequencing of the virus has paved the way for the use of omics technologies and an integrative technique in combating the pandemic. In general, the advancement of omics technology during this pandemic has been fascinating and has contributed a significant role to the science of health biotechnology in general and omics and bioinformatics in particular.Keywords: bioinformatics, coronavirus, COVID-19, omics, SARS COV-2","PeriodicalId":514464,"journal":{"name":"Molecular and Cellular Biomedical Sciences","volume":" 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140387306","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":"Angiotensin-Converting Enzyme Genetic Polymorphism rs4343 as Risk of Diabetic Nephropathy in Jambi-Malay Population","authors":"Elfiani Elfiani, Anggelia Puspasari, Cut Wulan Arif, C. Maharani, Z. Ali, N. Suhaimi, I. Effendi, S. Suprapti, N. Shafira","doi":"10.21705/mcbs.v8i1.410","DOIUrl":"https://doi.org/10.21705/mcbs.v8i1.410","url":null,"abstract":"Background: Diabetic nephropathy (DN) is one of the frequent complications of type II diabetes mellitus (T2DM) in Jambi province. Controlling blood glucose and blood pressure does not guarantee DN prevention, since genetic factors may also contribute to this disease. Multi-ethnic studies showed that one of the strongest genetic factors associated with DN was single nucleotide polymorphism rs4343 of angiotensin-converting enzyme (ACE) gene. Study regarding phenotype-genotype association of ACE rs4343 and DN has not yet been performed in Jambi Province, which is dominated by Malay ethnicity. This study was conducted to reveal the association between ACE rs4343 and the risk of DN in the Jambi-Malay population.Materials and methods: This was a cross-sectional study involving 75 subjects (44 with DN and 31 without DN) who suffered from T2DM and hypertension. DN was defined as albumin to creatinine ratio (ACR) ≥30 mg/g. Genotyping was performed with one-step tetra amplification refractory mutation system-polymerase chain reaction (PCR) using specific primer for ACE rs4343. Bivariate and multivariate analyses were performed to analyze the genetic risk for DN.Results: The bivariate analysis showed the proportion of DN subjects was higher than non-DN within the AG genotype (11:1) than within the AA (33:30) genotype. This difference was statistically significant (p=0.012; OR (95% CI): 10.00 (1.22-82.15)). Multivariate analysis showed that AG genotype (p=0.047; OR (95% CI): 10.04 (1.03-97.31)) and uncontrolled blood pressure (p=0.001; OR (95% CI): 6.72 (2.08-21.71)) were the risk factors of DN in the Jambi-Malay population.Conclusion: Polymorphism of ACE rs4343 is a risk factor of DN in the Jambi-Malay Population.Keywords: rs4343, angiotensin-converting enzyme gene, diabetic nephropathy, Malay, Jambi","PeriodicalId":514464,"journal":{"name":"Molecular and Cellular Biomedical Sciences","volume":" 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140387352","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}