Rosario Serrano's research while affiliated with University of Castilla-La Mancha and other places

... Mutation Stability increase í µí±¡ 1/2 Reference I91L 9-fold 18 h [61] N150H, K154T, Q319L, and M354I 72-fold 145 h [125] N150H, K154T, Q319L, M354I, and Q301P 75-fold 150 h [126] Combination of mutations at positions 50, 56, 61, 70, 94, 150, 222, 223, 264, and 331 122-fold 245 h [127] Disulfide mutant 350-fold 700 h [128] heterogeneous, tissue-specific glycosylation pattern was also observed [129]. It is hypothesized that PAI-1 circulates in both glycosylated and nonglycosylated states in vivo, depending on the cell type that expresses the protein [129, 135]. Despite the fact that glycosylation of PAI-1 is not a prerequisite for its activity [130], glycosylation status of PAI-1 is critically significant in the development of PAI-1 inhibitors [12, 28]. ...

... The use of synthetic inhibitors of MMPs and antibiotics were effectively found to reduce the vascular expression of MMPs, in particular MMP-2 and MMP-9 and delay the progression of atherosclerotic plaque (Rodriguez et al., 2007). However, it is noticed that long-term tetracycline use may cause side effects that limit their clinical use. ...

... Insulin is not merely the aetiology of belly fat but superimposes on the risk of cardiovascular disorders. In the elderly population, insulin resistance progressively increases with age leading to elevated type 2 diabetes incidence [52]. Alterations in body composition and insulin resistance correlate with dysregulation of physiological pathways with resultant obesity and diabetes [53], premature senescence, and cardiovascular disease risks [2,9,10,54]. ...

... Plasminogen-plasmin and the coagulation system are importantly involved in stroke [17]. As a fibrin degradation product, D-dimer is the most frequently used indicator to reflect the activation of the coagulation system. ...

... However, increases in tissue weights have been attributed to decreased lipolysis due to decreased amount of NE. While leptin increases glucose utilization in tissues with its central effect, it suppresses glucose utilization as well as lipogenesis in the white adipose tissue [13]. The removal of this inhibitory effect of leptin due to denervation may contribute to the increase in the tissue weight. ...

... It is produced and released into circulation primarily by endothelial cells but also by other cell types, including hepatocytes and adipocytes [107]. The latter explains why PAI-1 is a well-known adipocytokine, as its levels are markedly increased along with the accumulation of fat [45][46][47]108]. This possibly explains the correlation between elevated PAI-1 levels and obesity, a risk factor for T2D. ...

... The function of the IIS pathway in senescence was first discovered in mutants of the daf-2 gene encoding the insulin receptor in the nematode Caenorhabditis elegans (Kenyon et al., 1993;Kimura et al., 1997) and was confirmed subsequently in the fruit fly Drosophila melanogaster (Clancy et al., 2001;Tatar et al., 2003) and the mouse Mus musculus (Blüher et al., 2003;Holzenberger et al., 2003), thus demonstrating the universality of the senescence regulation by the IIS pathway. While there have been previous studies on how IIS signaling changes during the aging process (Serrano et al., 2005;Ismail et al., 2015;Augustin et al., 2017;Tanabe et al., 2017;Haroon et al., 2020), our under-standing of the cellular-level mechanisms in various organs remains limited. ...

... This inflamed adipose tissue (Sideri et al. 2015) would impact the intestinal function. Thus, GLUT12 upregulation in adipose tissue of old control mice could be related to the need of glucose uptake, which is deteriorated in aging (Reaven et al. 1989;Szoke et al. 2008), a condition in which insulin-induced GLUT4 translocation to the membrane is reduced (Villar et al. 2006). In line with the present results, we have previously demonstrated GLUT12 and GLUT4 decrease in adipose tissue of 5-monthold obese mice and lack of insulin response of the transporters (Gil-Iturbe et al. 2019a). ...

... Thrombin is a key enzyme in the coagulation cascade and a strong platelet activator via activation of proteaseactivated receptors (PAR1 and 4) on the cell membrane of the platelet, thus potentially acting as an important mediator in the procoagulant-prothrombotic state during acute myocardial infarction (AMI) [8]. Increased thrombin generation (TG) during AMI, as previously reported, is associated with a poor prognosis [9][10][11][12]. Thrombin is also associated with recruitment of bone marrow hematopoietic stem cells [13], including EPCs, thus serving as a key mediator in platelet function and hemostasis [7,14]. ...