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.

There has been growing interest in the potential anti-cancer activity of statins based on evidence of their anti-proliferative, pro-apoptotic, and radiosensitizing properties, but no studies have focused on the effects of statins on the chemoresistance. In spite of their direct cytostatic/cytotoxic effects on the cancer cells, statins via drug interactions may affect therapeutic effects of the chemotherapy agents and so cause chemoresistance in cancer cells. Here, we aim to present the molecular mechanisms underlying cytotoxic effects of statins on the cancer cells against those mechanisms by which statins may lead to chemoresistance, in order to clarify whether the positive effects of the co-treatment of statins on the efficiency of chemotherapeutic agents is due to the natural anti-cancer effects of statins or it is due to increasing the cellular concentrations of chemotherapy drugs in cancer cells.