Editorial: Vascular Dysfunction and Endocrine Disorders: Unraveling Interactions, Mechanisms, and Clinical Implications

Zhice Xu^1*Hong Liu²

• ¹Wuxi Maternity and Child Health Care Hospital, Wuxi, China
• ²University of California Davis, Davis, United States

For postmenopausal women, a cross-sectional study L. He, et al. using NHANES 2013-2014 data found that lower serum estradiol (E2) levels correlate with a higher prevalence of abdominal aortic calcification (AAC). Women in the lowest E2 tertile (2.12-3.57 pg/mL) had a 2.55-fold higher risk of prominent AAC (Kauppila score >5) compared to those in the highest tertile (7.06-38.4 pg/mL). This reinforces E2's role in maintaining cardiovascular health in postmenopausal women and supports E2 monitoring for early AAC prevention.Pregnancy-related endocrine disorders, such as gestational diabetes mellitus (GDM) and preeclampsia, are also explored for their vascular impacts. A review by J. Tang, et al. synthesized evidence that GDM disrupts maternal cardiovascular function, umbilical-placental perfusion, and fetal blood flow via mechanisms, including endothelial dysfunction, insulin resistance, and epigenetic modifications. These effects increase long-term cardiovascular risk for both mothers and offspring, highlighting the need for post-partum vascular surveillance in GDM patients.Preeclampsia-characterized by pregnancy-induced hypertension-was the focus of a transcriptomic study by Z Xu's team, which for the first time analyzed gene expression in pure placental microvessels (rather than whole placental tissue). The study identified 486 differentially expressed transcripts, with hub genes (e.g., ELMO1, YWHAE, IL6ST) down-regulated in preeclamptic small blood vessels. Functional tests revealed blunted vasoconstriction to angiotensin II and reduced vasodilation to nitric oxide donors in preeclamptic blood vessels-findings that suggest novel molecular targets for preeclampsia's vascular pathology.Prenatal exposure to glucocorticoids (GCs) is another key reproductive factor linked to offspring vascular dysfunction. A review by Q. Gao, et al. explained that while placental 11β-hydroxysteroid dehydrogenase 2 normally protects fetuses from maternal GCs by inactivating cortisol, adverse prenatal factors (e.g., stress, caffeine, synthetic GC use) can overwhelm this barrier. Excessive fetal GC exposure leads to long-term offspring cardiovascular issues, including hypertension and impaired vascular function-underscoring the need for cautious GC use in pregnancy. Type 2 diabetes mellitus (T2DM)-a hallmark endocrine-metabolic disorder-was the focus of three articles, each exploring distinct vascular sequelae. A pilot study (T. Hou, et al.) used 3D-arterial spin labeling (3D-ASL) to measure cerebral blood flow (CBF) in T2DM patients with mild cognitive impairment (MCI). Compared to T2DM patients without MCI, those with MCI had significantly lower CBF in the temporal, parietal, occipital, and hippocampal regions. Hippocampal CBF showed the highest diagnostic efficacy for MCI (AUC=0.813), positioning 3D-ASL as a promising tool for early MCI detection in T2DM.Another study (Y. Wang, et al.) investigated Isthmin-1 (ISM-1)-a novel adipokine-in T2DM patients with macrovascular complications (MACV). Serum ISM-1 levels were highest in MACV patients, followed by T2DM patients without MACV, and lowest in healthy controls. ISM-1 correlated positively with blood pressure, triglycerides, HbA1c, and insulin resistance (HOMA-IR), suggesting it may contribute to macrovascular disease by disrupting glucose-lipid metabolism.Acute ischemic stroke (AIS) in T2DM patients was explored in a retrospective study by L. Wang, et al., which found that HbA1c >6.5% is associated with severe hypercoagulability and heightened inflammation (via markers like the systemic immune-inflammation index, SII). HbA1c >6.5% was an independent predictor of hypercoagulability (OR=1.74), linking chronic hyperglycemia to thromboinflammation in AIS-findings that support tight glycemic control to improve stroke outcomes. This collection also offers critical insights into therapeutic interventions for vascular-endocrine disorders. For thin endometrium-a common cause of infertility in assisted reproductive technology (ART)-a network meta-analysis (F. Keng, et al.) of 18 randomized controlled trials (RCTs) compared six interventions. Platelet-rich plasma (PRP) ranked highest for improving clinical pregnancy rates (SUCRA=80.12%) and was among the top three for increasing endometrial thickness (SUCRA=68.14%), making it a promising first-line option for ART patients.In atherosclerosis-driven by endothelial dysfunction-a review (Y. Yan, et al.) categorized adipokines into protective (e.g., adiponectin, FGF21, CTRP9) and detrimental (e.g., leptin, resistin, FABP4) subsets. Targeting adipokines, such as enhancing protective adipokine signaling or inhibiting detrimental ones, could offer novel therapies for atherosclerosis-related cardiovascular disease (CVD).Finally, a review by P. Lan, et al. expanded the scope of vasoactive agents-traditionally used for cardiovascular regulation-by exploring their non-cardiovascular effects. Agents like angiotensin II and vasopressin influence endocrine functions (e.g., insulin secretion), the central nervous system, and gastrointestinal motility, emphasizing the need to monitor off-target effects in clinical practice. This Research Topic underscores the interconnectedness of vascular dysfunction and endocrine disorders, spanning metabolic syndrome, reproductive health, diabetes, and beyond. Key takeaways include the identification of novel biomarkers (e.g., RC/HDL-C, AIP, hippocampal CBF), the role of hormonal fluctuations (E2, GCs) in vascular health, and promising therapeutics (PRP, vitamin D supplementation, adipokine targeting).Future research should prioritize longitudinal studies to confirm causal relationships (e.g., between RC/HDL-C and hyperuricemia) and large-scale RCTs to validate interventions like PRP for thin endometrium. Additionally, integrating multi-omics approaches-such as transcriptomics (as in preeclamptic placental microvessels) and microbiomics (emerging in endometriosis research: Endometriosis-associated infertility, insights into pathogenesis and precision therapeutics)-will deepen understanding of underlying mechanisms.By bridging basic science and clinical practice, this Research Topic provides a foundation for personalized strategies to prevent, diagnose, and treat vascular-endocrine comorbidities-ultimately improving patient outcomes and advancing the field of integrative cardiovascular-endocrine medicine.