The extracellular matrix (ECM) serves as a dynamic biological framework that orchestrates cellular behavior through biomechanical and biochemical cues, playing a pivotal role in tissue homeostasis and repair. Despite significant advancements in biomaterial design, current regenerative strategies often fail to fully replicate the ECM's complexity, leading to suboptimal healing outcomes. This review comprehensively examines ECM biology and its application in biomaterial engineering, highlighting structural-functional relationships, integrin-mediated signaling, and ECM remodeling mechanisms in wound healing. We analyze diverse biomaterial classes—including ECM-based scaffolds, synthetic polymers, natural biomaterials, bioceramics, and composites—focusing on their design principles, fabrication techniques, degradation profiles, and clinical applications. Key challenges such as immunogenicity, vascularization, mechanical mismatch, and regulatory hurdles are critically evaluated. Innovations in decellularization, biofunctionalization, and advanced manufacturing (e.g., 3D bioprinting, electrospinning) are discussed as promising avenues to enhance biomimicry and therapeutic efficacy. Furthermore, we explore clinically approved ECM-derived products and underscore the need for standardized protocols to bridge translational gaps. By integrating emerging research with clinical perspectives, this review provides a roadmap for developing next-generation ECM-inspired biomaterials that address unmet needs in regenerative medicine, emphasizing interdisciplinary collaboration to optimize safety, functionality, and patient outcomes.

Background: Type 2 diabetes mellitus (T2DM) is an increasing metabolic disorder mostly resulting from unhealthy lifestyles. T2DM patients are prone to develop heart conditions such as coronary artery disease (CAD) which is a major cause of death in the world. Most clinical symptoms emerge at the advanced stages of CAD; therefore, establishing new biomarkers detectable in the early stages of the disease is crucial to enhance the efficiency of treatment. Recently, a significant body of evidence has shown alteration in miRNA levels associate with dysregulated gene expression occurring in T2DM and CAD, highlighting significance of circulating miRNAs in early detection of CAD arising from T2DM. Therefore, it seems crucial to establish a link between the miRNAs prognosing value and development of CAD in T2DM.Aim: This study provides an overview on the alterations of the circulatory miRNAs in T2DM and various CADs and consider the potentials of miRNAs as biomarkers prognosing CADs in T2DM patients.Materials and Methods: Literature search was conducted for miRNAs involved in development of T2DM and CAD using the following key words: “miRNAs”, “Biomarker”, “Diabetes Mellitus Type 2 (T2DM)”, “coronary artery diseases (CAD)”. Articles written in the English language.Result: There has been shown a rise in miR‐375, miR‐9, miR‐30a‐5p, miR‐150, miR‐9, miR‐29a, miR‐30d, miR‐34a, miR‐124a, miR‐146a, miR‐27a, and miR‐320a in T2DM; whereas, miR‐126, miR‐21, miR‐103, miR‐28‐3p, miR‐15a, miR‐145, miR‐375, miR‐223 have been shown to decrease. In addition to T2DM, some miRNAs such as mirR‐1, miR‐122, miR‐132, and miR‐133 play a part in development of subclinical aortic atherosclerosis associated with metabolic syndrome. Some miRNAs increase in both T2DM and CAD such as miR‐1, miR‐132, miR‐133, and miR‐373‐3‐p. More interestingly, some of these miRNAs such as miR‐92a elevate years before emerging CAD in T2DM.Conclusion: dysregulation of miRNAs plays outstanding roles in development of T2DM and CAD. Also, elevation of some miRNAs such as miR‐92a in T2DM patients can efficiently prognose development of CAD in these patients, so these miRNAs can be used as biomarkers in this regard.

Background: Cardiovascular diseases (CVDs) are the leading cause of mortality globally, often linked to oxidative stress. MicroRNAs (miRNAs) have emerged as significant regulators of oxidative stress within the cardiovascular system.Objective: This review examines the complex relationship between miRNAs and oxidative stress, clarifying their effects on gene expression pathways related to ROS production and detoxification in CVDs.Methods: From August to October 2024, we conducted a comprehensive search of PubMed, Scopus, Web of Science, and Google Scholar for studies published between 2014 and 2024 investigating the role of miRNAs in oxidative stress and cardiovascular diseases.Results: Specific miRNAs have been identified as critical regulators in the pathophysiology of CVDs, with distinct expression patterns correlated with conditions such as hypertension, coronary artery disease, and heart failure. For instance, miR‐21 exacerbates oxidative stress by targeting genes essential for redox homeostasis, while miR‐210 promotes endothelial cell survival under hypoxic conditions by mitigating ROS levels.Conclusion: The reciprocal relationship between miRNAs and oxidative stress highlights the potential for therapeutic interventions targeting miRNA expression and activity in managing CVDs. Understanding these molecular mechanisms is vital for developing innovative strategies to address oxidative damage in cardiac tissues and improve cardiovascular health outcomes.

Obesity and osteoporosis are interrelated global health challenges, both characterized by dysregulated bone metabolism and adipose tissue dynamics, contributing to increased fracture risk and systemic complications. Emerging evidence underscores the pivotal role of microRNAs (miRNAs) as regulatory molecules governing the intricate balance between adipogenesis and osteogenesis, thereby providing a molecular link between these two conditions. Both disorders are characterized by intricate alterations in bone metabolism and adipose tissue dynamics, which increase the risk of fractures and systemic complications. Recent advancements in molecular biology have identified miRNAs as crucial regulators of these disorders, influencing the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts (bone-forming cells) and adipocytes (fat-storing cells). This review provides a comprehensive analysis of the dual role of miRNAs in modulating osteogenesis and adipogenesis, with a particular focus on their implications in disease progression and therapeutic strategies. It first explores how specific miRNAs regulate critical energy metabolism, inflammation, and bone remodeling pathways. By integrating insights from molecular biology, endocrinology, and clinical practice, the review highlights the therapeutic potential of miRNA-based interventions. Targeting specific miRNAs could restore the balance between adipogenesis and osteogenesis, offering innovative approaches to simultaneously address obesity and osteoporosis. These proposed strategies hold promise for improving patient outcomes by mitigating fracture risk, enhancing bone density, and addressing metabolic dysfunctions associated with obesity. Ultimately, future research should focus on translating these molecular insights into clinical applications to develop effective therapies that tackle the complex interplay between these prevalent conditions.

Background: Coronary Artery Disease (CAD) has long been recognized as a global health issue. Inflammation, Fibrinolysis and Oxidative Stress play an important role in the disruption of plaques leading to CAD. Markers that reflect this pathophysiologic mechanism may have prognostic value. Objective: To estimate the serum concentrations of high-sensitivity C-reactive protein (hs-CRP), sialic acid (SA), vitronectin (VN), plasminogen activator inhibitor-1 (PAI-1), oxidized low density lipoprotein (OX-LDL) and malondialdehyde (MDA) with significant prognostic value in patients with CAD. Methods: The markers included, hs-CRP, SA, VN, PAI-1, OX-LDL and MDA, were compared between 160 angiographically diagnosed CAD patients and 20 age- and sex-matched healthy individuals. The subjects were divided into 4 groups according to angiography results, and association between all risk factors of CAD was studied. Serum levels of SA, VN, PAI-1, and OX-LDL were measured by enzyme-linked immunosorbent assay (ELBA); MDA was measured based on reaction with thiobarbituric acid (TBA); and hs-CRP level was estimated by immunoturbidimetry using a commercial kit. The diagnostic value of these variables was further assessed by ROC curve analysis. Multiple logistic regression was used to evaluate the diagnostic power of the combination. Furthermore, p < 0.05 was considered as significant. Results: Serum levels of hs-CRP, SA, VN, PAI-1, and OX-LDL were significantly higher in patient groups compared to control group (p < 0.001). Using both normal and CAD patients as subjects, ROC analysis was performed. The cutoff for OX-LDL, MDA, PAI-1, VN, hs-CRP and SA was 2.67 (ug/mL), 5.49 (mmol/mL), 67 (ng/mL), 254 (ng/mL), 3.4 (mg/dL), 7/89 (mg/dL), respectively. Eventually, the complete diagnostic efficacy was classified as: SA, hs-CRP, PAI-1, OX-LDL, MDA and VN. Conclusion: Serum levels SA, hs-CRP, VN, PAI-1, OX-LDL and MDA may be predictive of adverse cardiovascular outcomes. Interestingly, these analyses can help as diagnostic and monitoring markers in CAD patients.

MicroRNAs (miRNAs) are small, noncoding RNA molecules that play a vital role in regulating gene expression, especially in the differentiation of mesenchymal stem cells (MSCs) into vascular smooth muscle cells (VSMCs). MSCs hold considerable promise for vascular repair and regenerative medicine, given their ability to differentiate into smooth muscle cells (SMCs) under specific molecular cues. Recent studies have shown that miRNAs, through complex regulatory networks, influence MSC differentiation by targeting essential signaling pathways and modulating the expression of differentiation markers, underscoring the intricate roles of these molecules in cellular development. This review comprehensively examines the functions of various miRNAs in MSC differentiation, focusing on miR-143 and miR-145, which are upregulated by transforming growth factor beta 1 (TGF-β1), a key growth factor in SMC development. These miRNAs enhance differentiation by promoting the expression of SMC markers, including α-smooth muscle actin (α-SMA) and calponin, and by inhibiting factors that preserve MSCs in an undifferentiated state. This review further discusses the roles of miR-503, which supports SMC differentiation through SMAD7 inhibition via the TGF-β pathway, and miR-222-5p, which counteracts differentiation by downregulating ROCK2 and α-SMA. By highlighting these regulatory mechanisms, this review aims to clarify the bidirectional and multifaceted role of miRNAs in VSMC differentiation. This study offers insights into the therapeutic potential of miRNA-mediated MSC differentiation for vascular repair and regeneration, ultimately contributing to improved cardiovascular outcomes.