The burden of cardiovascular diseases and the critical role of acute coronary syndrome (ACS) in their progression underscore the need for effective diagnostic and prognostic tools. Biomarkers have emerged as crucial instruments for ACS diagnosis, risk stratification, and prognosis assessment. Among these, high-sensitivity troponin (hs-cTn) has revolutionized ACS diagnosis due to its superior sensitivity and negative predictive value. However, challenges regarding specificity, standardization, and interpretation persist. Beyond troponins, various biomarkers reflecting myocardial injury, neurohormonal activation, inflammation, thrombosis, and other pathways are being explored to refine ACS management. This review article comprehensively explores the landscape of clinically used biomarkers intricately involved in the pathophysiology, diagnosis, and prognosis of ACS (i.e., troponins, creatine kinase MB (CK-MB), B-type natriuretic peptides (BNP), copeptin, C-reactive protein (CRP), interleukin-6 (IL-6), d-dimers, fibrinogen), especially focusing on the prognostic role of natriuretic peptides and of inflammatory indices. Research data on novel biomarkers (i.e., endocan, galectin, soluble suppression of tumorigenicity (sST2), microRNAs (miRNAs), soluble oxidized low-density lipoprotein receptor-1 (sLOX-1), F2 isoprostanes, and growth differentiation factor 15 (GDF-15)) are further analyzed, aiming to shed light on the multiplicity of pathophysiologic mechanisms implicated in the evolution of ACS. By elucidating the complex interplay of these biomarkers in ACS pathophysiology, diagnosis, and outcomes, this review aims to enhance our understanding of the evolving trajectory and advancements in ACS management. However, further research is necessary to establish the clinical utility and integration of these biomarkers into routine practice to improve patient outcomes.

Novel Biomarkers and Their Role in the Diagnosis and Prognosis of Acute Coronary Syndrome

Oral cancer is the sixth most prevalent type of cancer worldwide and third in India out of the different cancer types identified. Mouth and oral cancers collectively refer to cancers of the buccal cavity, lips, oropharynx, hypopharynx, and larynx. Genetic anomalies, the upregulation of several proteins, the deregulation of tumor-suppressive and oncogenes, and risk factors like alcohol and tobacco consumption are a few examples of the known irregularities that contribute to the development of oral cancer through the accumulation of various carcinogenic substances. Oral cancer is caused and developed by multiple molecular and cellular pathways such as PI3K/AKT/mTOR, Ras-Raf-MEK-ERK pathway, Wnt signaling, NF-κB pathway, Hippo pathway, etc. In addition, various genes including TP53, PTEN, CDKN2A, HRAS, PIK3CA, NOTCH1, IRF6, TP63, etc. are also involved in this malignancy. Therefore, it is crucial to have a deep understanding of these pathways to properly understand the development of oral cancer. This concise review focuses on compiling together various signaling and molecular pathways accountable for oral carcinoma development. URN:NBN:sciencein.cbl.2024.v11.652 

Signaling and molecular pathways implicated in oral cancer: A concise review

Reactive oxygen species (ROSs) are byproducts of normal cellular metabolism and play pivotal roles in various physiological processes. Disruptions in the balance between ROS levels and the body’s antioxidant defenses can lead to the development of numerous diseases. Glutathione peroxidase 3 (GPX3), a key component of the body’s antioxidant system, is an oxidoreductase enzyme. GPX3 mitigates oxidative damage by catalyzing the conversion of hydrogen peroxide into water. Beyond its antioxidant function, GPX3 is vital in regulating metabolism, modulating cell growth, inducing apoptosis and facilitating signal transduction. It also serves as a significant tumor suppressor in various cancers. Recent studies have revealed aberrant expression of GPX3 in several non-neoplastic diseases, associating it with multiple pathological processes. This review synthesizes the current understanding of GPX3 expression and regulation, highlighting its extensive roles in noncancerous diseases. Additionally, this paper evaluates the potential of GPX3 as a diagnostic biomarker and explores emerging therapeutic strategies targeting this enzyme, offering potential avenues for future clinical treatment of non-neoplastic conditions. 

Insights into the Role of Glutathione Peroxidase 3 in Non-Neoplastic Diseases

Revisiting tuberculosis screening: An insight to complementary diagnosis and prospective molecular approaches for the recognition of the dormant TB infection in human and cattle hosts.

Bovine tuberculosis is an important worldwide disease mainly related to cattle, although it also affects other mammals, including humans. In recent years, there have been considerable advances in the knowledge of the immune response mechanisms underlying the interaction of Mycobacterium bovis, the main agent of bovine tuberculosis, with its hosts. In this review we describe the most recent findings on the cattle immune response to M. bovis, particularly regarding trained innate immune responses and γδ T cells, that could support the development of vaccines and diagnostic tools to control this disease.

Recent advances in non-specific immune memory against bovine tuberculosis.

This article sheds light on the various scaffolds that can be used in the designing and development of novel synthetic compounds to create DPP-4 inhibitors for the treatment of type 2 diabetes mellitus (T2DM). This review highlights a variety of scaffolds with high DPP-4 inhibition activity, such as pyrazolopyrimidine, tetrahydro pyridopyrimidine, uracil-based benzoic acid and esters, triazole-based, fluorophenyl-based, glycinamide, glycolamide, β-carbonyl 1,2,4-triazole, and quinazoline motifs. The article further explains that the potential of the compounds can be increased by substituting atoms such as fluorine, chlorine, and bromine. Docking of existing drugs like sitagliptin, saxagliptin, and vildagliptin was done using Maestro 12.5, and the interaction with specific residues was studied to gain a better understanding of the active sites of DPP-4. The structural activities of the various scaffolds against DPP-4 were further illustrated by their inhibitory concentration (IC50) values. Additionally, various synthesis schemes were developed to make several commercially available DPP4 inhibitors such as vildagliptin, sitagliptin and omarigliptin. In conclusion, the use of halogenated scaffolds for the development of DPP-4 inhibitors is likely to be an area of increasing interest in the future. 

Insight into Structure Activity Relationship of DPP-4 Inhibitors for Development of Antidiabetic Agents

Differential gene expression in Mycobacterium bovis challenged monocyte-derived macrophages of cattle.

This study identified a total of 28 genetic loci (comprising 31 genes), which were found to be altered in oral cancer patients having a habit of tobacco smoking. Three loci, that is, 17p13.1 (TP53), 9p21.3 (CDKN2A), and 9q34.3 (NOTCH1) were found to be modified and common in three records whereas one locus, that is, 3q26.32 (PIK3CA) was found to be modified and common in two records. This study suggests that oral cancer patients should be categorized into different subgroups based on (i) genetic signatures, and (ii) smoking status, then the treatment strategies for each group should be precisely defined. 

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/imt2.44

Impact of tobacco smoking on oral cancer genetics—A next‐generation sequencing perspective

Acute myocardial infarction (AMI) is a severe disease with elevated morbidity and mortality rate worldwide. This is attributed to great losses of cardiomyocytes, which can trigger the alteration of gene expression patterns. Although several attempts have been made to assess the AMI biomarkers, to date their role in rescuing myocardial injury remains unclear. Therefore, the current study investigated three independent microarray-based gene expression datasets from AMI patients (n = 85) and their age–sex-matched healthy controls (n = 70), to identify novel gene signatures that might be involved in cardioprotection. The differentially expressed genes (DEGs) were analyzed using ‘GEO2R’, and weighted gene correlation network analysis (WGCNA) was performed to identify biomarkers/modules. We found 91 DEGs, of which the number of upregulated and downregulated genes were 22 and 5, respectively. Specifically, we found that the deregulated genes such as ADOR-A3, BMP6, VPS8, and GPx3, may be associated with AMI. WGCNA revealed four highly preserved modules among all datasets. The ‘Enrichr’ unveiled the presence of miR-660 and STAT1, which is known to affect AMI severity. Conclusively, these genes and miRNA might play a crucial role the rescue of cardiomyocytes from severe damage, which could be helpful in developing appropriate therapeutic strategies for the management of AMI.

https://www.mdpi.com/2073-4425/13/12/2321/pdf?version=1670580964

Transcriptomic Profiling Unravels Novel Deregulated Gene Signatures Associated with Acute Myocardial Infarction: A Bioinformatics Approach

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