Background: The human bioaccumulation of micro- and nano-plastics (MNPs) is increasingly being recognised in the aetiology and pathophysiology of human disease. Objective: This systematic scoping review aims to provide a comprehensive investigation of studies examining the impacts of MNPs on the human cardiovascular system. Methods: Five databases (PubMed, SCOPUS, CINAHL, Web of Science and EMBASE) were systematically searched. Results: Forty-six articles were identified, 13 of which investigated the presence of MNPs within the human cardiovascular system, including atherosclerotic plaques, saphenous vein tissue, thrombi and venous blood. The effect of MNPs on cell lines suggest MNPs are cytotoxic, immunotoxic, and genotoxic. Significance: The findings of this review, when evaluated together with additional studies utilising animal models, suggest MNPs may contribute to global cardiovascular morbidity and mortality. In particular, the ability of MNPs to induce endothelial damage, oxy-LDL formation, foam cell development and apoptosis, as well as to alter the clotting cascade, has potential implications for vascular diseases. In addition, MNPs may play a role in the aetiology and progression of congenital heart abnormalities, infective pathologies and cardiomyopathies. Despite an increasing awareness of the ability for MNPs to result in cardiovascular disease and dysfunction, a limited amount of research has been conducted to date characterising the presence of MNPs in the human cardiovascular system. Reseach is required to understand the extent of this rapidly emerging issue and to develop strategies that will support clinicians to appropriately manage and educate their patients in the future.

Drug repurposing provides a cost‐effective and time‐saving approach to cancer therapy. Aripiprazole (ARI), a third‐generation antipsychotic, has shown potential anticancer properties by modulating pathways central to tumor progression and resistance. This scoping review systematically examines evidence on ARI's anticancer effects, mechanisms of action, and translational potential. A systematic search of PubMed, EMBASE, SCOPUS, and Web of Science was conducted following PRISMA‐ScR guidelines. Eligible studies included in vitro, in vivo, and clinical investigations. Data on cancer types, pathways, assays, and outcomes were extracted and synthesized to identify trends and gaps. Of 588 screened studies, 23 met inclusion criteria, spanning cancer types such as breast, colorectal, lung, and brain cancers. ARI modulates key pathways like PI3K/AKT/mTOR and Wnt/β‐catenin, induces apoptosis through mitochondrial dysfunction and ER stress, and overcomes drug resistance by inhibiting P‐glycoprotein activity and expression. It exhibits tumor‐suppressive effects in vivo and synergizes with chemotherapy and radiotherapy. Retrospective population studies suggest ARI's prolactin‐sparing properties may reduce the risk of hormone‐sensitive cancers such as breast and endometrial cancer compared to antipsychotics with stronger dopamine receptor blockade. Additionally, ARI's ability to target multiple Hallmarks of Cancer highlights its promise as a repurposed anticancer agent. However, current evidence is primarily preclinical and observational, with limited clinical validation. Large‐scale cohort studies and prospective trials are essential to confirm its efficacy and address translational challenges. By bridging these gaps, ARI could emerge as a valuable adjunctive therapy in oncology, leveraging its safety profile and versatility to address unmet needs in cancer treatment.

Drug repurposing offers a cost‐effective and time‐efficient strategy for identifying new cancer therapies. Sertraline, a widely prescribed selective serotonin reuptake inhibitor (SSRI), has shown promising anticancer properties through modulation of key pathways involved in tumor survival, stress adaptation, and therapeutic resistance. This scoping review systematically evaluates the current evidence on sertraline's anticancer mechanisms, efficacy, and translational potential. A systematic search of PubMed, EMBASE, Scopus, and Web of Science was conducted in accordance with PRISMA‐ScR guidelines. Eligible studies included in vitro, in vivo, and clinical investigations. Data on cancer types, mechanisms, assays, and outcomes were extracted and synthesized. Of 97 screened articles, 67 met inclusion criteria, comprising 56 preclinical studies, nine population‐based studies, and two mixed‐methods reports. Sertraline induces apoptosis via mitochondrial dysfunction, caspase activation, and Bcl‐2 downregulation, disrupts autophagy and the unfolded protein response, and impairs serine/glycine metabolism through SHMT inhibition. It also suppresses oncogenic signaling via mTOR and TCTP modulation. In vivo studies confirmed tumor growth inhibition in various cancer models, including breast, lung, glioblastoma, and liver. Sertraline enhances the efficacy of chemotherapy, radiotherapy, and targeted therapies by sensitizing resistant cells, modulating immune responses, and impairing metabolic recovery. Retrospective studies suggest no increased cancer risk with SSRI use and hint at protective associations in select malignancies. While current evidence is predominantly preclinical, sertraline's multi‐targeted action and established safety profile support its candidacy for repurposing. Further translational research and biomarker‐driven clinical trials are warranted to validate its therapeutic niche and optimize its integration into oncology.

Background: Human bioaccumulation of micro- and nanoplastics (MNPs) is increasingly being recognised in the aetiology and pathophysiology of human disease. This systematic scoping review aims to provide a comprehensive investigation of studies examining the presence and effects of MNPs on the human pulmonary system. Methods: A scoping review was conducted in line with JBI guidelines. Five databases (PubMed, SCOPUS, CINAHL, Web of Science and EMBASE) were systematically searched. Results: Sixty-eight articles were identified, with fifteen reporting the presence of MNPs in human respiratory tissues and fluids. The data reported in the remaining toxicology-focused studies suggest that MNPs induce widespread cellular dysfunction in pulmonary-related human cell lines. Exposure to MNPs was associated with significant cytotoxicity, genotoxicity and altered metabolic activity, including mitochondrial damage, increased reactive oxygen species and reduced membrane potential. Functionalised and smaller particles had more pronounced effects. Conclusions: The reported presence of MNPs, coupled with their biological toxicity, represents a growing global health concern. Evidence suggests MNPs may contribute to the rising burden of pulmonary disease worldwide, including cancer, COPD, interstitial lung disease and ARDS. Urgent international research is needed to characterise exposure pathways, develop standardised detection methods and understand the long-term health implications of MNP inhalation across the lifespan.

Aim: Mebendazole (MBZ), a benzimidazole anthelmintic with established clinical use, has emerged as a repurposing candidate for primary brain tumours due to its multimodal anticancer actions and central nervous system penetrance. This systematic review synthesizes preclinical and clinical evidence evaluating MBZ's efficacy, mechanisms of action and translational relevance. Methods: This systematic review was conducted in accordance with the Joanna Briggs Institute (JBI) methodology. Systematic searches were performed in PubMed, EMBASE, SCOPUS and Web of Science using predefined eligibility criteria. A total of 22 studies were included (17 preclinical and five clinical/population). Results: Preclinical work across glioblastoma, diffuse midline glioma, medulloblastoma and meningioma demonstrates consistent tumour growth suppression and survival extension via microtubule depolymerization, kinase inhibition, angiogenesis blockade, Hedgehog pathway interference, apoptosis/pyroptosis induction and impairment of DNA repair. MBZ also potentiates standard therapies, enhancing the effects of alkylators, radiotherapy and autophagy inhibitors. Efficacy was influenced by formulation, with polymorph C demonstrating superior brain penetration and tolerability. Additional delivery strategies, including efflux inhibition, intranasal microemulsions and nanosuspensions, further improved exposure. Clinically, MBZ was generally tolerable at high oral doses in early‐phase studies, but evidence of efficacy remained modest, inconsistent and inconclusive. Conclusion: MBZ shows broad preclinical anticancer activity and acceptable tolerability in early human studies, but current clinical evidence does not demonstrate meaningful efficacy in brain tumour patients. Further well‐designed comparative trials with clear formulation reporting and integrated pharmacokinetic and biomarker analyses are needed.

Background The human bioaccumulation of micro- and nano-plastics (MNPs) is increasingly being recognised in the aetiology and pathophysiology of human disease. This systematic scoping review provides a comprehensive investigation of studies examining the impacts of MNPs on the human cardiovascular system. Methods Five databases (PubMed, SCOPUS, CINAHL, Web of Science and EMBASE) were systematically searched. Results Thirty-four articles were identified, six of which investigated the presence of MNPs within the human cardiovascular system, including atherosclerotic plaques, saphenous vein tissue, and venous blood. The effect of MNPs on cell lines suggest MNPs are cytotoxic, immunotoxic, and genotoxic. Discussion The findings of this review, when evaluated together with additional studies utilising animal models, strongly suggest MNPs currently contribute to global cardiovascular morbidity and mortality. In particular, the ability of MNPs to induce endothelial damage, oxy-LDL formation, foam cell development and apoptosis, as well as altering the clotting cascade, has potential implications for vascular diseases. In addition, MNPs may play a role in the aetiology and progression of congenital heart abnormalities, infective pathologies and cardiomyopathies. Conclusion Despite an increasing awareness of the ability of MNPs to result in cardiovascular disease and dysfunction, a limited amount of research has been conducted to date characterising the presence of MNPs in the human cardiovascular system. Research is required to understand the extent of this rapidly emerging issue and to develop strategies that will support clinicians to appropriately manage and educate their patients about this issue in the future.