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The Role of the Microbiota and the Application of Probiotics in Reducing the Risk of Cardiovascular Diseases
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Raquel Bedani, Susana Marta Isay Saad
Wang et al. (2017), investigating the role of sodium butyrate (NaBu) in angiotensin II (Ang II)-induced hypertension in an experimental model with Sprague-Dawley rats, verified that intramedullary infusion of NaBu exerts an antihypertensive action, probably by suppressing the (pro)renin receptor mediated intrarenal renin-angiotensin system. A clinical trial conducted by Roshanravan et al. (2017) in adults with type 2 diabetes mellitus showed that the supplementation with sodium butyrate capsules, inulin powder and inulin + butyrate capsules during 45 days significantly reduced diastolic blood pressure compared to the placebo group.
Gestational diabetes mellitus
Published in Moshe Hod, Vincenzo Berghella, Mary E. D'Alton, Gian Carlo Di Renzo, Eduard Gratacós, Vassilios Fanos, New Technologies and Perinatal Medicine, 2019
Silvia Vannuccini, Federico Mecacci
Several biomarkers have been tested for GDM, especially during the first trimester, in order to perform an early diagnosis of the disease (35,36). These include markers of glucose metabolism, insulin resistance, inflammation, fat tissue activity, and placental function. In the last years, novel markers have been investigated, such as vitamin D, soluble (pro)renin receptor, glycosylated fibronectin, and microRNAs (37) (Table 6.3). However, their role should be further investigated in prospective studies, also evaluating their relevance when integrating with clinical predictive models. Furthermore, the recent introduction of omics technologies, such as proteomics and metabolomics, will open the opportunity to understand the flow of information that underlies diseases (38).
The Renin—Angiotensin—Aldosterone System
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Ulrike M. Steckelings, Thomas Unger
In 1996 and continued in 2002, a membrane receptor was reported which binds renin and prorenin (20,21). Upon binding of renin/prorenin, this so-called (pro-)renin receptor [(P)RR] reacts in two ways: a) an increase in enzymatic activity of both renin and prorenin resulting in enhanced production of Ang I/Ang II, and b) activation of signalling cascades in an Ang II—independent way, which includes nuclear translocation of the transcription factor promyelocytic leukaemia zinc finger (PLZF) and phosphorylation of the mitogen-activated protein (MAP) kinases ERK1 and ERK2 (21,22). The (patho-)physiological relevance and consequences of (pro)renin binding to the (P)RR are still not completely elucidated, and data are controversial (23). Recent evidence rather suggests that the primary role of the (P)RR is RAAS independent but involves a role in the canonical and noncanonical Wnt signalling pathways as well as V-ATPase dependent intracellular vesicle trafficking, vesicular acidification and autophagy (23).
Local ocular renin–angiotensin–aldosterone system: any connection with intraocular pressure? A comprehensive review
Published in Annals of Medicine, 2020
Mervi Holappa, Heikki Vapaatalo, Anu Vaajanen
Renin is a highly specific aspartyl protease; it activates the RAAS cascade by hydrolysing its only known substrate: angiotensinogen (AGT) to angiotensin I (Ang I) [29]. AGT is the precursor of all of the angiotensin peptides; AGT is mainly synthesized and released into the bloodstream from the liver, e.g. in response to inflammation, insulin and oestrogen [30]. Interestingly, some organs, such as heart and kidney, are also known to produce AGT [30]. Renin, on the other hand, is mainly synthesized, stored and released in renal juxtaglomerular cells in response to decreased arterial BP, reductions in sodium levels or increased activity of sympathetic nervous system [31,32]. Renin is synthesized as an inactive form called prorenin [33]. The pro-sequence is first cleaved by kallikrein, cathepsin B or proconvertase before fully active renin is released into the circulation [31,33]. Renin, and its less active form prorenin, can mediate vasoconstrictive effects via (pro)renin receptor ((P)RR) [33–35].
Efficient isolation and culture of endothelial cells from venous malformation using the Rho-associated protein kinase inhibitor Y27632
Published in Journal of Plastic Surgery and Hand Surgery, 2018
Takashi Satoh, Masakazu Kurita, Hirotaka Suga, Hitomi Eto, Mine Ozaki, Akihiko Takushima, Kiyonori Harii
Y27632 inhibits the differentiation of mesenchymal cells through the inhibition of Rho kinase-MLC signalling. In our research, Y27632 revealed the same effects on the ECs and non-ECs from VM, supporting the above-cited report by Joo et al. [16]. Y27632 inhibits the contraction of vascular smooth muscle [19,20], cell migration [21–23], and the control of gene expression [24,25] through the Rho kinase signalling pathway. Y27632 also markedly diminished the dissociation-induced apoptosis of ESCs during the culture [26]. A Rho kinase inhibitor is useful for the primary culture of undifferentiated cells such as ESCs and keratinocytes. However, it has not been clear whether a Rho kinase inhibitor can be used for the primary culture of differentiated cells such as ECs. Our present findings revealed that Y27632 is very useful for the primary culture of ECs. From that perspective, there may be the possibility that the Y27632-sensitive ECs are somewhat stem-like. Further study will be needed to reveal it. Meanwhile, recent work by Siljee et al. [27] suggests the expression of the pro-renin receptor (PRR) on some of the EC from VM, given the interplay between PRR and the Rho-associated protein kinase [28]. Y27632, a Rho-associated protein kinase inhibitor, would be an important tool to elucidate the aetiology of VM. Furthermore, recent studies revealed somatic activating mutations in PIK3CA cause sporadic VM in mouse models [29–31]. These studies can be helpful to the elucidation of the aetiology of VM and to the study of the target therapies in VM.
Aliskiren and valsartan in combination is a promising therapy for hypertensive renal injury in rats
Published in Clinical and Experimental Hypertension, 2018
Despite its inhibition of the enzymatic activity of renin, aliskiren increases the biosynthesis and secretion of renin and prorenin, which might induce renal tissue damage (5) by activating the (pro)renin receptor [(P)RR]. Additionally, the (P)RR may amplify renin-induced Ang II-dependent effects; renin bound to the (P)RR gains fivefold enhanced catalytic activity versus soluble renin (6). Studies in genetically modified animals over-expressing (P)RR suggest a direct role for (P)RR in cardiovascular and renal pathologies since rats over-expressing (P)RR in vascular smooth-muscle cells develop high blood pressure and those with an ubiquitous over-expression of (P)RR have glomerulosclerosis and proteinuria (7).