Subarachnoid hemorrhage (SAH) is most commonly seen in patients over 55 years of age and often results in a loss of many productive years. SAH has a high mortality rate, and survivors often suffer from early and secondary brain injuries. Understanding the pathophysiology of the SAH is crucial in identifying potential therapeutic agents. One promising target for the diagnosis and prognosis of SAH is circulating microRNAs, which regulate gene expression and are involved in various physiological and pathological processes. In this review, we discuss the potential of microRNAs as a target for diagnosis, treatment, and prognosis in SAH.

Background Subarachnoid hemorrhage (SAH) is a life-threatening condition with high mortality and significant neurological morbidity, often complicated by delayed cerebral ischemia (DCI) and vasospasm. Heme metabolites such as biliverdin (BV) are implicated in SAH-induced vascular dysfunction, yet the role of biliverdin reductase-A (BVR-A), an enzyme that reduces BV to bilirubin, remains underexplored. This study investigates the contribution of BV and oxidative post-translational modifications of BVR-A to vasospasm development. Methods We used a murine model of BV injection into the subarachnoid space and analyzed its effects on vasospasm, microthrombosis, neuronal apoptosis, and microglial activation. Additionally, human plasma and cerebrospinal fluid (CSF) samples from patients with SAH with and without vasospasm were evaluated for BVR-A expression and oxidative modifications using immunoprecipitation and western blot techniques. Results BV injection in the murine model induced significant vasospasm, increased microthrombosis, neuronal apoptosis, and a reactive morphological shift in microglia. In human samples, oxidative modifications of BVR-A were significantly raised in plasma from patients with SAH with vasospasm compared with those without, despite similar BVR-A expression levels. No significant differences in oxidative modifications were observed in CSF samples. Conclusion This study shows a novel role of BV in vasospasm development and identifies oxidative modifications of BVR-A as potential modulators of SAH pathology. These findings suggest that BV and altered BVR-A activity may serve as biomarkers or therapeutic targets for improving outcomes in patients with SAH.

Glioblastoma (GBM) is the most common and aggressive primary brain tumor, characterized by poor prognosis and a median survival of 12–18 months despite standard therapies such as surgery, radiation, and temozolomide chemotherapy. Its high cellular heterogeneity, along with complex mechanisms of therapy resistance, presents significant challenges for effective treatment. Conventional systemic chemotherapy is limited by the blood–brain barrier (BBB), systemic toxicity, and insufficient drug penetration into the tumor microenvironment. Emerging therapeutic strategies aim to overcome these barriers through novel chemotherapeutic agents, targeted therapies, immunotherapies, and smart drug delivery systems. Endovascular drug delivery, particularly super-selective intra-arterial cerebral infusion (SSIACI), offers a minimally invasive approach to directly target the tumor vasculature, potentially increasing drug concentration at the tumor site while reducing systemic exposure. Complementary techniques, such as MR-guided focused ultrasound, hyperosmotic disruption, and nanoparticle-based carriers, are being explored to enhance BBB penetration and retention of therapeutics within the tumor. Ongoing clinical trials and translational studies provide insights into optimizing these approaches, with future directions focused on precision medicine, biomarker-driven patient selection, and combination therapies. Integrating endovascular strategies with innovative chemotherapies and immunotherapies may transform GBM management, but further research is required to establish their efficacy and safety in clinical practice.

Background: Delayed cerebral ischemia remains a major cause of morbidity after aneurysmal subarachnoid hemorrhage (SAH), and effective therapies beyond nimodipine are lacking. Adropin, an endogenous peptide that regulates endothelial function and nitric oxide signaling, has shown neurovascular protective effects in experimental SAH. However, its efficacy when administered at clinically relevant delayed time points and in severe SAH remains unclear. Methods: A severe double‐injection SAH model was induced in male C57BL/6 mice. Synthetic adropin or vehicle was administered beginning 6 or 12 hours after SAH, with repeat dosing according to experimental end points. Outcomes included eNOS (endothelial nitric oxide synthase) signaling, blood–brain barrier integrity, cerebral vasospasm, microvascular thrombosis, neuronal apoptosis, and neurobehavioral performance. Additional studies were conducted in energy homeostasis–associated knockout mice and tamoxifen‐induced brain endothelial‐specific adropin deletion. Statistical analyses were performed using Prism 10. Results: Endogenous adropin expression and eNOS signaling were reduced 24 hours after SAH. Adropin administration restored total eNOS expression. Adropin preserved tight junction integrity, selectively restoring occludin expression, and significantly reduced microvascular thrombosis. When administered 6 hours after SAH, adropin attenuated delayed cerebral vasospasm, reduced neuronal apoptosis, improved recognition memory and mitigated anxiety‐like behavior at 1 month post SAH. In contrast, adropin administered 12 hours after SAH conferred partial and inconsistent behavioral benefit and did not significantly reverse vasospasm. Adropin attenuated vasospasm and improved behavioral outcomes in energy homeostasis–associated knockout mice. Endothelial‐specific adropin deletion did not exacerbate vasospasm, and systemic adropin administration did not further improve vessel diameter in this model. Conclusions: Adropin confers robust neurovascular protection after severe SAH when administered within a clinically relevant early therapeutic window. These findings highlight adropin as a promising candidate for mitigating endothelial dysfunction, vasospasm, and long‐term neurological deficits following SAH, with timing of intervention playing a critical role in therapeutic efficacy.

Subarachnoid hemorrhage (SAH) is most commonly seen in patients over 55 years of age and often results in a loss of many productive years. SAH has a high mortality rate, and sur-vivors often suffer from early and secondary brain injuries. Understanding the pathophysiology of the SAH is crucial to identifying potential therapeutic agents. One promising target for diagno-sis and prognosis of SAH is circulating microRNAs, which regulate gene expression and are in-volved in various physiological and pathological processes. In this review, we discuss the poten-tial of microRNAs as a target for diagnosis, treatment, and prognosis in SAH.