Hypoxia is a hallmark of the tumor microenvironment (TME), and it plays a crucial role in the occurrence and progression in vascular tumors. Under hypoxic conditions, hypoxia-inducible factor 1-alpha (HIF-1α) is stabilized, inducing changes in the expression of various target genes involved in angiogenesis, metabolism, and cell survival. This includes the upregulation of pro-angiogenic factors like VEGF, which promotes the formation of dysfunctional blood vessels, contributing to the worsening of the hypoxic microenvironment. At the same time, hypoxia induces a metabolic shift toward glycolysis, even in the presence of oxygen, supporting tumor cell survival and proliferation by providing necessary energy and biosynthetic precursors. This review discusses the molecular mechanisms by which hypoxia regulates angiogenesis and metabolic reprogramming in vascular tumors, highlighting the intricate link between these processes, and explores potential therapeutic strategies to target these pathways in order to develop effective treatment strategies for patients.

Hemoporfin-mediated photodynamic therapy (HMME-PDT) has demonstrated significant advantages in the treatment of Port-wine stains (PWSs). However, the therapeutic efficacy of HMME-PDT remains suboptimal in a subset of patients. Somatic mosaic mutations in GNAQ (c.548G>A, p. R183Q) are frequently detected in endothelial cells (ECs) of lesions and represent a common pathogenic mechanism. In this study, we successfully established an in vitro model of PWSs by introducing the GNAQ p. R183Q mutation into HUVECs using lentiviral infection. Our results revealed that GNAQ p. R183Q mutation enhanced ECs proliferation, migration, and angiogenesis. Moreover, the mutation augmented anti-apoptotic mechanisms, thereby conferring heightened resistance to HMME-PDT-induced apoptosis. Residual angiogenic activity persisted following HMME-PDT treatment. These effects are likely mediated by activation of the angiopoietin-2 (ANGPT2)/TIE2/PI3K/AKT signaling axis. Knockdown of ANGPT2 partly reversed these phenotypic alterations and significantly enhanced the efficacy of HMME-PDT. The combination of HMME-PDT with anti-ANGPT2 therapy holds promise for enhancing therapeutic efficacy, suppressing pathological angiogenesis, and ameliorating the clinical manifestations of PWSs.

Background: Blue rubber bleb nevus syndrome (BRBNS) is a rare venous malformation disorder. Currently, there is no standard therapy for this disease. However, lauromacrogol, a sclerosant extensively utilized in the management of vascular malformations, has been applied in the treatment of BRBNS. Research on the combined therapy of sirolimus and lauromacrogol for the treatment of BRBNS remains limited.Case summary: Here, we report the case of a 12-year-old girl diagnosed with BRBNS. The patient presented with chronic anemia and skin “hemangioma.” The examinations showed severe anemia, along with decreased serum iron and ferritin levels. Magnetic resonance imaging showed abnormal nodular lesions in various parts of the intestine. The patient was treated with a combination of endoscopic sclerotherapy using lauromacrogol and oral sirolimus. After 1 year of treatment, the patient showed no signs of anemia or gastrointestinal tract bleeding.Conclusion: BRBNS is a rare disorder that is often misdiagnosed, especially by inexperienced pediatricians. The combination of oral sirolimus with endoscopic lauromacrogol has demonstrated efficacy in reducing lesion size and elevating hemoglobin levels.

Objective: This study reports a rare and life-threatening case of a giant congenital hemangioma with arteriovenous fistula in a neonate and describes its clinical management and outcomes. Method: A female neonate with a giant right forearm hemangioma with arteriovenous fistula, detected prenatally at 23 weeks, was managed by a multidisciplinary team. Postnatally, the infant developed severe pulmonary hypertension and active bleeding from the mass. Diagnosis was confirmed via computed tomography angiography and arteriography. Emergency intervention with combined embolization coil and sclerotherapy was performed, followed by oral propranolol therapy. Results: Following the combined intervention and pharmacotherapy, the condition of the infant improved significantly. The severe pulmonary hypertension resolved, and the tumor size progressively reduced. Conclusion: Congenital hemangioma combined with arteriovenous malformation can lead to severe, life-threatening complications. A prompt, multidisciplinary approach involving embolization, sclerotherapy, and pharmacotherapy can achieve favorable outcomes, underscoring the importance of early recognition and integrated perinatal management.

Background: In newborns, infantile hemangiomas (IHs) in the airway can present with rare life-threatening complications associated with airway obstruction, even without cutaneous hemangioma.Case report: Our female newborn exhibited stridor 1 day after her birth. Furthermore, 7 days after birth, she was admitted to the local hospital to receive phototherapy for neonatal jaundice. However, her stridor was not noted as being related to IH by the clinician during her hospitalization. She was transferred to our hospital at 14 days old because her stridor and condition deteriorated with severe breathlessness and respiratory failure. Computed tomography and flexible bronchoscopy identified obstructive airway IHs. Although a combination therapy of propranolol and corticosteroids was prescribed for 2 weeks, she still needed invasive mechanical ventilation. After a discussion by the multidisciplinary team, endoscopic resection was carried out to resolve her airway obstruction at 30 days old, but it failed. Finally, transcatheter interventional sclerotherapy successfully resolved her clinical conditions at 60 days old. She was discharged and received follow-up with propranolol treatment. Her clinical symptoms of airway IHs were completely resolved 1 year later.Conclusions: Airway IHs can rarely present with life-threatening conditions associated with airway obstruction without cutaneous hemangioma in newborns. This case report highlights that propranolol is the cornerstone treatment for airway IHs. For the first time, our findings suggest that transcatheter interventional sclerotherapy can be a valid additional treatment option.

Background: Sturge–Weber syndrome (SWS) is a rare congenital neurocutaneous disorder. Timely diagnosis and management remain challenging, particularly when intracranial hemorrhage (IH) occurs as a rare but serious complication. Case presentation: A young child developed IH after minor head trauma and presented with irritability, vomiting, gait instability, and lethargy. His symptoms progressed to recurrent focal motor seizures, status epilepticus, and hemiplegia. Initial CT showed a hematoma in the left frontal lobe, but SWS was not recognized immediately. Gadolinium-enhanced magnetic resonance imaging showed multiple gyriform enhancing linear shadows and leptomeningeal enhancement along the cortex extending into the sulci, consistent with pial angiomatosis. The diagnosis of SWS was established on the basis of the extensive port-wine stain (PWS), seizures, and neuroimaging findings. Intravenous midazolam relieved the seizures and restored consciousness, followed by sequential oral levetiracetam and valproic acid therapy. During follow-up, he remained seizure-free for more than two years while receiving anticonvulsants and low-dose aspirin, with only mild right hemiparesis. Conclusion: IH may be the first recognized neurological manifestation of previously undiagnosed SWS. In children with facial PWS and acute neurological symptoms, prompt neuroimaging may facilitate diagnosis and guide individualized management.