Diabetic foot complications represent a major global health burden and arise from a multifactorial interaction between neuropathy, ischemia, infection, and impaired wound repair. Increasing evidence suggests that, beyond traditional vascular and metabolic risk factors, endocrine dysregulation plays a central role in shaping vascular dysfunction and tissue vulnerability in patients with diabetes. This narrative review provides an updated overview of the endocrine–vascular axis in the development, progression, and healing of diabetic foot ulcers (DFUs), integrating evidence from experimental and clinical studies identified through targeted searches of PubMed, Embase, and Scopus. We examine how alterations in insulin signaling, relative glucagon excess, adipokine imbalance, dysregulation of stress hormones, and thyroid dysfunction interact with chronic hyperglycemia, dyslipidemia, mitochondrial dysfunction, and low-grade inflammation to impair endothelial homeostasis. These disturbances promote oxidative stress, reduce nitric oxide bioavailability, and compromise microvascular perfusion, thereby creating a pro-ischemic and pro-inflammatory tissue environment that limits angiogenesis, extracellular matrix (ECM) remodeling, immune coordination, and effective wound repair. By linking pathophysiological mechanisms to clinical relevance, this review highlights potential biomarkers of endocrine–vascular dysfunction, implications for risk stratification, and emerging therapeutic perspectives targeting metabolic optimization, endothelial protection, and hormonal modulation. Finally, key knowledge gaps and priority areas for future translational and clinical research are discussed, supporting the development of integrated endocrine-based strategies aimed at improving DFU prevention, healing outcomes, and long-term limb preservation in patients with diabetes.

Carotid artery stenting (CAS) is an established revascularization option for patients with carotid disease at high surgical risk. Periprocedural cerebral embolization remains a clinical concern, and plaque prolapse, the extrusion of atherosclerotic material through the stent struts into the lumen, has emerged as an actionable mechanism directly linked to embolic events and adverse neurological outcomes. This narrative review provides a structured, practice-oriented framework addressing one specific question: how can plaque prolapse be prevented during CAS? Drawing on prospective registries, comparative cohort studies and intravascular imaging analyses based on optical coherence tomography (OCT) and intravascular ultrasound (IVUS), we discuss the main determinants of prolapse risk, plaque morphology, procedural variables and device selection, converging on dual-layer micromesh stent (DLMS) technology as the most advanced device-based solution available. Pooled clinical data indicate a 30-day stroke rate of approximately 1.4% when DLMSs are used in combination with embolic protection, and OCT studies confirm reduced prolapse compared with single-layer stents. Prevention requires an integrated strategy combining lesion-specific characterisation, optimised technique and tailored device selection, while standardised imaging definitions and adequately powered randomised trials with hard clinical endpoints remain research priorities.