Search Results (7)

Background/Objectives: Central serous chorioretinopathy (CSCR) is a common retinopathy that can present with other concurrent diseases; thus, further research into the prevalence of other ocular comorbidities in eyes with CSCR is required. Methods: This retrospective, multicentric, cross-sectional observational study reviewed the charts of 9157 patients. Of them, 579 (6.32%) patients and 766 eyes had an additional ocular comorbidity, in addition to CSCR, in at least one subject eye. Results: The baseline best-corrected visual acuity (BCVA) of the subjects eyes was 0.49 ± 0.36 logMAR. The average BCVA of subject eyes with coexisting macular diseases was 0.50 logMAR, while the corresponding BCVA of subject eyes with coexisting peripheral disease was 0.55 logMAR. The most prevalent coexisting macular diseases were non-proliferative diabetic retinopathy (26.8%), non-exudative age-related macular degeneration (AMD) (7.6%) and hypertensive retinopathy (3.0%). The most prevalent coexisting non-macular diseases were lattice degeneration (8.9%), optic atrophy (5.1%), rhegmatogenous retinal detachment (1.70%) and optic disc pit (1.7%). The odds of having a comorbid disease in the same eye as CSCR were statistically significant for branch retinal vein occlusion (OR 11.56, p-value = 0.02) and non-exudative AMD (OR 2.06; p-value = 0.01); additionally, there was a trend towards significance for idiopathic polypoidal choroidal vasculopathy (OR 4.43; p-value = 0.05) when compared to the eyes without CSCR. Conclusions: Certain diseases are more likely to coexist in eyes with CSCR. Additionally, eyes with CSCR may have statistically significant odds of certain diseases when compared to eyes without CSCR. Full article

Antiphospholipid syndrome (APS) is an autoimmune prothrombotic condition characterized by venous thromboembolism, arterial thrombosis, and pregnancy morbidity. Among neurological manifestations, arterial thrombosis is only one of the possible associated clinical and neuroradiological features. The aim of this review is to address from a neurovascular point of view the multifaceted range of the arterial side of APS. A modern neurovascular approach was proposed, dividing the CNS involvement on the basis of the size of affected arteries, from large to small arteries, and corresponding clinical and neuroradiological issues. Both large-vessel and small-vessel involvement in APS were detailed, highlighting the limitations of the available literature in the attempt to derive some pathomechanisms. APS is a complex disease, and its neurological involvement appears multifaceted and not yet fully characterized, within and outside the diagnostic criteria. The involvement of intracranial large and small vessels appears poorly characterized, and the overlapping with the previously proposed inflammatory manifestations is consistent. Full article

Systemic Sclerosis (SSc) is a heterogeneous autoimmune disease characterized by widespread vasculopathy, the presence of autoantibodies and the progressive fibrosis of skin and visceral organs. There are still many questions about its pathogenesis, particularly related to the complex regulation of the fibrotic process, and to the factors that trigger its onset. Our recent studies supported a key role of N-formyl peptide receptors (FPRs) and their crosstalk with uPAR in the fibrotic phase of the disease. Here, we found that dermal fibroblasts acquire a proliferative phenotype after the activation of FPRs and their interaction with uPAR, leading to both Rac1 and ERK activation, c-Myc phosphorylation and Cyclin D1 upregulation which drive cell cycle progression. The comparison between normal and SSc fibroblasts reveals that SSc fibroblasts exhibit a higher proliferative rate than healthy control, suggesting that an altered fibroblast proliferation could contribute to the initiation and progression of the fibrotic process. Finally, a synthetic compound targeting the FPRs/uPAR interaction significantly inhibits SSc fibroblast proliferation, paving the way for the development of new targeted therapies in fibrotic diseases. Full article

Cellular senescence, a state of permanent cell cycle arrest in response to endogenous and exogenous stimuli, triggers a series of gradual alterations in structure, metabolism, and function, as well as inflammatory gene expression that nurtures a low-grade proinflammatory milieu in human tissue. A growing body of evidence indicates an accumulation of senescent neurons and blood vessels in response to stress and aging in the retina. Prolonged accumulation of senescent cells and long-term activation of stress signaling responses may lead to multiple chronic diseases, tissue dysfunction, and age-related pathologies by exposing neighboring cells to the heightened pathological senescence-associated secretory phenotype (SASP). However, the ultimate impacts of cellular senescence on the retinal vasculopathies and retinal vascular development remain ill-defined. In this review, we first summarize the molecular players and fundamental mechanisms driving cellular senescence, as well as the beneficial implications of senescent cells in driving vital physiological processes such as embryogenesis, wound healing, and tissue regeneration. Then, the dual implications of senescent cells on the growth, hemostasis, and remodeling of retinal blood vessels are described to document how senescent cells contribute to both retinal vascular development and the severity of proliferative retinopathies. Finally, we discuss the two main senotherapeutic strategies—senolytics and senomorphics—that are being considered to safely interfere with the detrimental effects of cellular senescence. Full article

Background: Wilm’s tumor 1 gene (WT1) is a transcription factor with versatile cellular functions in embryonic development, the maintenance of adult tissue functions, and regeneration. WT1 is known to be regulated by progesterone and it is abundantly expressed in endometrium, but its function is unclear. Design: in this observational and descriptive study, WT1 expression was detected by immunohistochemical staining in endometrium of various physiological and pathological conditions. Result: WT1 was detected in endometrial stromal cells and vascular smooth muscle cells, in both proliferative and secretory phases of menstrual cycles. WT1 appeared increased in vascular smooth muscle cells in spiral artery in early pregnancy and it was also detected in regenerative endothelial cells and smooth muscle cells in decidual vasculopathy at term. WT1 expression appeared decreased in endometrial stromal cells in adenomyosis (endometriosis). Conclusion: WT1 potentially links the hormonal effects on endometrial decidualization and may play a role in gestational vascular transformation during pregnancy and restoration after pregnancy. Full article

Vasculogenesis and angiogenesis are physiological mechanisms occurring throughout the body. Any disruption to the precise balance of blood vessel growth necessary to support healthy tissue, and the inhibition of abnormal vessel sprouting has the potential to negatively impact stages of development and/or healing. Therefore, the identification of key regulators of these vascular processes is critical to identifying therapeutic means by which to target vascular-associated compromises and complications. Nuclear receptors are a family of transcription factors that have been shown to be involved in modulating different aspects of vascular biology in many tissues systems. Most recently, the role of nuclear receptors in ocular biology and vasculopathies has garnered interest. Herein, we review studies that have used in vitro assays and in vivo models to investigate nuclear receptor-driven pathways in two ocular vascular diseases associated with blindness, wet or exudative age-related macular degeneration, and proliferative diabetic retinopathy. The potential therapeutic targeting of nuclear receptors for ocular diseases is also discussed. Full article

Hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant inherited disease characterised by multisystemic vascular dysplasia. Heritable pulmonary arterial hypertension (HPAH) is a rare but severe complication of HHT. Both diseases can be the result of genetic mutations in ACVLR1 and ENG encoding for proteins involved in the transforming growth factor-beta (TGF-β) superfamily, a signalling pathway that is essential for angiogenesis. Changes within this pathway can lead to both the proliferative vasculopathy of HPAH and arteriovenous malformations seen in HHT. Clinical signs of the disease combination may not be specific but early diagnosis is important for appropriate treatment. This review describes the molecular mechanism and management of HPAH and HHT. Full article