Portal hypertension (PHT) is a major cause of liver cirrhosis. The formation of portosystemic collateral vessels and splanchnic vasodilation contribute to the development of hyperdynamic circulation, which in turn aggravates PHT and increases the risk of complications. To investigate the changes in mesenteric arterioles in PHT, cirrhotic rat models were established by ligating the common bile ducts. After 4 weeks, the cirrhotic rats suffered from severe PHT and splanchnic hyperdynamic circulation, characterized by increased portal pressure (PP), cardiac output (CO), cardiac index (CI), and superior mesenteric artery (SMA) flow. Mesenteric arterioles in cirrhotic rats displayed remarkable vasodilation, vascular remodeling, and hypocontractility. RNA sequencing was performed based on these findings. A total of 1,637 differentially expressed genes (DEGs) were detected, with 889 up-regulated and 748 down-regulated genes. Signaling pathways related to vascular changes were enriched, including the vascular endothelial growth factor (VEGF), phosphatidylinositol-3-kinase-AKT (PI3K-AKT), and nuclear factor kappa light chain enhancer of activated B cells (NF-κB) signaling pathway, among others. Moreover, the top ten hub genes were screened according to the degree nodes in the protein-protein interaction (PPI) network. Functional enrichment analyses indicated that the hub genes were involved in cell cycle regulation, mitosis, and cellular response to oxidative stress and nitric oxide (NO). In addition, promising candidate drugs for ameliorating PHT, such as resveratrol, were predicted based on hub genes. Taken together, our study highlighted remarkable changes in the mesenteric arterioles of cirrhotic rats with PHT. Transcriptome analyses revealed the potential molecular mechanisms of vascular changes in splanchnic hyperdynamic circulation.

Alzheimer\'s disease (AD) is a progressive neurodegenerative disorder that manifests as cognitive deficits and memory decline, especially in old age. Several biomarkers have been developed to monitor AD progression. Given that the retina and brain share some similarities including features related to anatomical composition and neurological functions, the retina is closely associated with the progression of AD. Herein, we review the evidence of retinal dysfunction in AD, particularly at the early stage, together with the underlying molecular mechanisms. Furthermore, we compared the retinal pathologies of AD and other ophthalmological diseases and summarized potential retinal biomarkers measurable by existing technologies for detecting AD, providing insights for the future development of diagnostic tools.

OBJECTIVE: To evaluate the vascular anatomy of eyes with Best vitelliform macular dystrophy (BVMD) using optical coherence tomography angiography (OCTA).
METHODS: This retrospective case-control study enrolled 11 consecutive BVMD patients and 13 age-matched healthy participants. Both eyes of each participant were imaged using a macular OCTA scan (3 × 3 mm) by 70-kHz 840-nm spectral-domain OCT. The flow signal was calculated using the split-spectrum amplitude-decorrelation angiography (SSADA) algorithm.
RESULTS: Qualitative analysis showed uneven hypo- and hyperintense signal changes at the choriocapillary level in OCTA images of BVMD patients. Quantitative analysis showed significant reductions in the flow density of the superficial vascular layer (whole: 49.2% vs. 53.9%, p < 0.001) and the choriocapillary flow area (5.1 vs. 5.5 mm2, p = 0.02) in BVMD patients compared to controls. The choriocapillary flow area in the postvitelliform group was reduced compared to that of the vitelliform group. There was a statistically significant association between choriocapillary flow area and superficial vascular flow density (p = 0.045), choriocapillary flow area and foveal avascular zone area (p = 0.03).
CONCLUSIONS: Vascular changes in BVMD were apparent in the choriocapillary layer. The changes became more striking in late stages of the disease. OCTA provides useful quantitative measurements for staging and monitoring the progression of BVMD.