Uterine fibroids are the most common benign tumors in women, with abnormal uterine bleeding (AUB) as the main reported symptom. Additionally, an association between fibroids and infertility has been established, especially if the fibroid protrudes in the uterine cavity. Hormonal therapy is associated with side-effects and as well as hysterectomy, which is incompatible with a desire to conceive. To improve treatment, it is essential to unravel the etiology of fibroid-related symptoms. We aim to evaluate endometrial angiogenesis in women with fibroids, with and without AUB, and the influence of pharmaceutical therapies in these patients. Furthermore, we explore the possible role of altered angiogenesis in patients with fibroids and infertility. We performed a systematic review according to PRISMA-guidelines (PROSPERO: CRD42020169061), and included 15 eligible studies. Endometrial expression of vascular endothelial growth factor (VEGF) and adrenomedullin was increased in patients with fibroids. This suggests aberrant angiogenesis, potentially involving disturbed vessel maturation, resulting in immature and fragile vessels. Treatment with gonadotropin-releasing hormone agonist, ulipristal acetate, and continuous oral contraception pills reduced several angiogenic parameters, including VEGF. If infertile and fertile patients with fibroids were compared, a significant decreased expression of the bone morphogenetic protein/Smad-protein pathway was found, possibly caused by the increased expression of transforming growth factor-beta. For future therapeutic development, these different angiogenic pathways could be of interest as possible targets to treat fibroid-related symptoms.

Abnormal uterine bleeding (AUB) has a significant socioeconomic impact since it considerably impacts quality of life. Therapeutic options are frequently based on trial and error and do not target disease aetiology. Pathophysiological insight in this disease is required for the development of novel treatment options. If no underlying cause is found for the AUB (e.g. fibroids, adenomyosis, polyps), endometrial-AUB (AUB-E) is usually caused by a primary endometrium disorder. When AUB is induced by prescribed (exogenous) hormones, it is classified as iatrogenic-AUB (AUB-I). Considering vascular modulation and function, AUB-E and AUB-I both could potentially result from abnormal vascularization in the endometrium due to alterations in the process of angiogenesis and vascular maturation.
We aim to investigate the fundamental role of angiogenesis and vascular maturation in patients with AUB and hypothesize that aberrant endometrial angiogenesis has an important role in the aetiology of both AUB-E and AUB-I, possibly through different mechanisms.
A systematic literature search was performed until September 2021 in the Cochrane Library Databases, Embase, PubMed, and Web of Science, with search terms such as angiogenesis and abnormal uterine bleeding. Included studies reported on angiogenesis in the endometrium of premenopausal women with AUB-E or AUB-I. Case reports, letters, reviews, editorial articles, and studies on AUB with causes classified by the International Federation of Gynecology and Obstetrics as myometrial, oncological, or infectious, were excluded. Study quality was assessed by risk of bias, using the Cochrane tool and the Newcastle-Ottawa Scale.
Thirty-five out of 2158 articles were included. In patients with AUB-E, vascular endothelial growth factor A and its receptors (1 and 2), as well as the angiopoietin-1:angiopoietin-2 ratio and Tie-1, were significantly increased. Several studies reported on the differential expression of other pro- and antiangiogenic factors in patients with AUB-E, suggesting aberrant vascular maturation and impaired vessel integrity. Overall, endometrial microvessel density (MVD) was comparable in patients with AUB-E and controls. Interestingly, patients with AUB-I showed a higher MVD and higher expression of proangiogenic factors when compared to controls, in particular after short-term hormone exposure. This effect was gradually lost after longer-term exposure, while alterations in vessel maturation were observed after both short- and long-term exposures.
AUB-E and AUB-I are most likely associated with aberrant endometrial angiogenesis and impaired vessel maturation. This review supports existing evidence that increased proangiogenic and decreased antiangiogenic factors cause impaired vessel maturation, resulting in more fragile and permeable vessels. This matches our hypothesis and these mechanisms appear to play an important role in the pathophysiology of AUB-E and AUB-I. Exploring the alterations in angiogenesis in these patients could provide treatment targets for AUB.

This review provides a comprehensive insight into the angiogenic profile of hypertensive and normotensive pregnancies compromised by HIV infection. Furthermore, we evaluate the economic implementation of the sFlt-1/PlGF ratio and review the reports on therapeutic apheresis in limiting sFlt-1 production.
In preeclampsia, an increased expression of sFlt-1 triggers angiogenic imbalance. Women of African ancestry have high levels of angiogenic factors than other racial groups. The sFlt-1/PlGF ratio shows promise in the early assessment of preeclampsia, while sFlt-1 apheresis restores angiogenic imbalance. Studies suggest antiretroviral therapy does not impact the angiogenic shift in preeclampsia development. The angiogenic profile in pregnant women of different races influences preeclampsia development. Despite the opposing immune response in HIV infection and preeclampsia, the HIV tat protein strongly mimics vascular endothelial growth factor (VEGF); hence, it is plausible to assume that HIV infection may ameliorate the angiogenic imbalance in preeclampsia.

BACKGROUND: Psoriasis is a chronic disease of inflammatory nature. It involves autoimmune mechanism and the systemic diseased state is created by the interaction of immune system, autoantigens and variety of environmental triggers. It is a complex skin disease which involves participation of numerous factors, making it multifactorial in nature. The main characteristics include proliferation of keratinocytes, increase in dermal vascularity and infiltrated immune cells. Among all factors, vascular alterations present a significant feature of the disease and angiogenesis seems to have an important role in giving rise to psoriasis phenotype. In the early phases of psoriasis there occurs sprouting of new blood vessels which disappear with disease clearance. Psoriatic lesions show highly altered vascular network in the form of numerous enlarged, tortuous and hyperpermeable cutaneous blood vessels. Secretion of various pro-angiogenic growth factors promote the expansion of vascular network in psoriatic skin cells. In addition to pro-angiogenic growth factors, pro-inflammatory cytokines also contribute to this process by activating endothelial cells and exerting pro-angiogenic action as well. Angiogenesis, in psoriasis display a close association of vascular endothelium activation, angiogenesis, inflammation and lesional skin, as is demonstrated by in vivo models.
OBJECTIVE: The present review discusses angiogenesis as the central process in the evolution of psoriasis and summarizes various angiogenic mediators and their respective roles in the development of psoriasis.
CONCLUSIONS: Anti-angiogenic therapies targeting vasoproliferation may represent a valid approach for the development of anti-psoriatic drugs and further development in this field can pave way to new fields of treatment. Such therapies could be at par to those directly targeting inflammation.

Brain-specific angiogenesis inhibitor (BAI) family of proteins are basically putative G-protein-coupled receptors with wide spectrum of cellular activities. These BAIs exhibit intricate and complex nature of modulatory activities that researchers are only now beginning to understand. Here we mainly focus on the regulatory activities of a prominent member of BAI family, BAI1, with respect to its role in inflammation, tumorigenesis and phagocytosis. The emerging knowledge on cell- and site-specific function of BAI1 makes it both versatile and promising candidate for studies relating to cancer and host immune response. This review collectively specifies and comprehends important findings of BAI1 from several studies and provides latest insight to explore its properties for possible biomedical therapeutics.

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Vascular manifestations can be seen early in the pathogenesis of inflammatory rheumatic diseases. Animal experiments, laboratory and clinical findings indicated that acute or long-term vibration exposure can induce vascular abnormalities. Recent years, in addition to Raynaud\'s phenomenon (RP), vibration as a risk factor for other rheumatic diseases has also received corresponding considered. This review is concentrated upon the role of vibration in the disease of systemic sclerosis (SSc). In this review, we are going to discuss the main mechanisms which are thought to be important in pathophysiology of vascular injury under the three broad headings of \"vascular\", \"neural\" and \"intravascular\". Aspects on the vibration and vascular inflammation are briefly discussed. And the epidemiological studies related to vibration studies in SSc and other rheumatic diseases are taken into account.

The introduction of new therapeutic agents into clinical practice of ovarian cancer, in addition to the role of surgery and chemotherapy, has been the subject of numerous studies because this tumor remains worldwide the most lethal gynecological cancer. It is now known that angiogenesis plays a vital role for ovarian physiology, but also in ovarian carcinogenesis and so it has become the main target of ovarian cancer treatment. In this review, the most common molecular pathways of angiogenesis have been investigated leading to the identification of novel targets, including monoclonal antibodies and tyrosine kinase inhibitors. The fundamental targets of anti-angiogenic drugs are vascular endothelial growth factor receptor and its ligand, but also platelet-derived growth factor, fibroblast growth factor and angiopoietin. Moreover, improved knowledge of angiogenic process allowed the discovery of other molecules, such as semaphorins, neuropilins, clusterin, some transcriptional factors, and the identification of features, including stemness, epithelial-mesenchymal transition, downregulation of certain microRNAs, the alteration of immune system, that contribute to angiogenesis and possibly to resistance mechanisms. The following patent and literature review aim to highlight recent findings of approved and novel anti-angiogenic drugs that make the treatment of patients with ovarian cancer a rapidly growing field of oncology.

BACKGROUND: Tissue biomarkers could pivotally improve clinical outcome prediction following prostate cancer therapy. Clinically, prostate cancer is managed by diverse treatment modalities whose individual influence on a biomarker\'s predictive ability is not well understood and poorly investigated in the literature.
OBJECTIVE: We conducted a systematic review to assess the predictive value of biomarkers in different treatment contexts in prostate cancer.
UNASSIGNED: A literature search was performed using the MeSH headings \"prostate neoplasms\" and \"biological markers\". Rigorous selection criteria identified studies correlating expression with clinical outcomes from primary androgen deprivation therapy (ADT), radical prostatectomy and radiotherapy (± neoadjuvant ADT).
RESULTS: Of 10,668 studies identified, 481 papers matched initial inclusion criteria. Following rescreening, 384 studies identified 236 individual tissue biomarkers, of which 29 were predictive on multivariate analysis in at least 2 independent cohorts. The majority were only tested in surgical cohorts. Only 8 predictive biomarkers were tested across all 3 treatments with Ki67 identified as universal predictive marker. p16 showed potential for treatment stratification between surgery and radiotherapy but needs further validation in independent studies.
CONCLUSIONS: Despite years of research, very few tissue biomarkers retain predictive value in independent validation across therapy context. Currently, none have conclusive ability to help treatment selection. Future biomarker research should consider the therapy context and use uniform methodology and evaluation criteria.

Tissue engineering is a newly emerging biomedical technology, which aids and increases the repair and regeneration of deficient and injured tissues. It employs the principles from the fields of materials science, cell biology, transplantation, and engineering in an effort to treat or replace damaged tissues. Tissue engineering and development of complex tissues or organs, such as heart, muscle, kidney, liver, and lung, are still a distant milestone in twenty-first century. Generally, there are four main challenges in tissue engineering which need optimization. These include biomaterials, cell sources, vascularization of engineered tissues, and design of drug delivery systems. Biomaterials and cell sources should be specific for the engineering of each tissue or organ. On the other hand, angiogenesis is required not only for the treatment of a variety of ischemic conditions, but it is also a critical component of virtually all tissue-engineering strategies. Therefore, controlling the dose, location, and duration of releasing angiogenic factors via polymeric delivery systems, in order to ultimately better mimic the stem cell niche through scaffolds, will dictate the utility of a variety of biomaterials in tissue regeneration. This review focuses on the use of polymeric vehicles that are made of synthetic and/or natural biomaterials as scaffolds for three-dimensional cell cultures and for locally delivering the inductive growth factors in various formats to provide a method of controlled, localized delivery for the desired time frame and for vascularized tissue-engineering therapies.