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The Renin Angiotensin System, Molecular, Geroscience and Aging-Related Disorders 2.0
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The Renin Angiotensin System, Molecular, Geroscience and Aging-Related Disorders 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 8229

Special Issue Editor

Prof. Satoru Eguchi

E-Mail Website
Guest Editor
Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA
Interests: cardiovascular signaling; angiotensin
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous special issue "The Renin Angiotensin System, Molecular, Geroscience and Aging-Related Disorders".

The renin angiotensin system (RAS) plays a key role in blood pressure regulation by controlling vascular smooth muscle constriction and renal water/sodium reabsorption. Disruption of RAS regulation occurs in individuals with cardiovascular disease (CVD) risk factors, leading to hypertension and associated complications. Aging is one of the major nonmodifiable risk factors for hypertension and other CVDs, which is exemplified in middle age individuals whose vasculature is more prematurely aged than that of their chronologically aged counterparts, and who therefore suffer from CVD development sooner. Recent research suggests that over-reactivity of the RAS plays a critical role in the pathogenesis of an accelerated aging phenotype seen in various diseases, such as neurodegenerative, cardiovascular, and metabolic disorders. While the exact mechanism by which RAS contributes to the development of these pathologies is not clear, it likely involves induction of premature senescence and senescence associated secretory phenotype (SASP). Disruption of organelle (i.e., mitochondria) quality control and proteostasis may also be affected in senescence-associated diseases, as these decline with age. Therefore, elucidating the molecular mechanism of the premature aging phenotype induced by the RAS would likely provide potential new therapeutic opportunities to maintain healthy aging and reduce the economic burden of aging diseases in the next century. Accordingly, the topics of this Special Issue include but are not limited to the recent findings in molecular mechanisms of the RAS in cellular aging, how the RAS influences age-related cardiovascular, metabolic, and neurological disorders, and translational evaluations on the findings.

Prof. Satoru Eguchi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Senescence
  • Biological aging
  • Early vascular aging (EVA)
  • Aortic stiffness
  • Senolytics
  • Longevity
  • Mitochondria
  • Proteotoxicity

Published Papers (3 papers)

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Research

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19 pages, 4347 KiB  
Article
Interaction between the Renin–Angiotensin System and Enteric Neurotransmission Contributes to Colonic Dysmotility in the TNBS-Induced Model of Colitis
by Mariana Ferreira-Duarte, Tiago Rodrigues-Pinto, Teresa Sousa, Miguel A. Faria, Maria Sofia Rocha, Daniela Menezes-Pinto, Marisa Esteves-Monteiro, Fernando Magro, Patrícia Dias-Pereira, Margarida Duarte-Araújo and Manuela Morato
Int. J. Mol. Sci. 2021, 22(9), 4836; https://doi.org/10.3390/ijms22094836 - 3 May 2021
Cited by 15 | Viewed by 2687
Abstract
Angiotensin II (Ang II) regulates colon contraction, acting not only directly on smooth muscle but also indirectly, interfering with myenteric neuromodulation mediated by the activation of AT1 /AT2 receptors. In this article, we aimed to explore which mediators and cells were [...] Read more.
Angiotensin II (Ang II) regulates colon contraction, acting not only directly on smooth muscle but also indirectly, interfering with myenteric neuromodulation mediated by the activation of AT1 /AT2 receptors. In this article, we aimed to explore which mediators and cells were involved in Ang II-mediated colonic contraction in the TNBS-induced rat model of colitis. The contractile responses to Ang II were evaluated in distinct regions of the colon of control animals or animals with colitis in the absence and presence of different antagonists/inhibitors. Endogenous levels of Ang II in the colon were assessed by ELISA and the number of AT1/AT2 receptors by qPCR. Ang II caused AT1 receptor-mediated colonic contraction that was markedly decreased along the colons of TNBS-induced rats, consistent with reduced AT1 mRNA expression. However, the effect mediated by Ang II is much more intricate, involving (in addition to smooth muscle cells and nerve terminals) ICC and EGC, which communicate by releasing ACh and NO in a complex mechanism that changes colitis, unveiling new therapeutic targets. Full article
(This article belongs to the Special Issue The Renin Angiotensin System, Molecular, Geroscience and Aging-Related Disorders 2.0)
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14 pages, 3180 KiB  
Article
Delayed Administration of Angiotensin Receptor (AT2R) Agonist C21 Improves Survival and Preserves Sensorimotor Outcomes in Female Diabetic Rats Post-Stroke through Modulation of Microglial Activation
by LaDonya Jackson-Cowan, Wael Eldahshan, Selin Dumanli, Guangkuo Dong, Sarah Jamil, Yasir Abdul, Waleed Althomali, Babak Baban, Susan C. Fagan and Adviye Ergul
Int. J. Mol. Sci. 2021, 22(3), 1356; https://doi.org/10.3390/ijms22031356 - 29 Jan 2021
Cited by 16 | Viewed by 2278
Abstract
About 70% of stroke victims present with comorbid diseases such as diabetes and hypertension. The integration of comorbidities in pre-clinical experimental design is important in understanding the mechanisms involved in the development of stroke injury and recovery. We recently showed that administration of [...] Read more.
About 70% of stroke victims present with comorbid diseases such as diabetes and hypertension. The integration of comorbidities in pre-clinical experimental design is important in understanding the mechanisms involved in the development of stroke injury and recovery. We recently showed that administration of compound C21, an angiotensin II type 2 receptor agonist, at day 3 post-stroke improved sensorimotor outcomes by lowering neuroinflammation in diabetic male animals. In the current study, we hypothesized that a delayed administration of C21 would also lower chronic inflammation post-stroke in diabetic female animals. Young female diabetic rats were subjected to 1 h of middle cerebral artery occlusion (MCAO). Three days post-stroke, rats were administered C21 or vehicle in drinking water at a dose of 0.12 mg/kg/day for 4 weeks. The impact of C21 on microglial polarization was analyzed by flow cytometry in vivo and in vitro. Compound 21 treatment improved fine motor skills after MCAO through modulation of the microglia/macrophage inflammatory properties. In addition, C21 increased M2 polarization and reduced the M1:M2 ratio in vitro. In conclusion, delayed administration of C21 downregulates post-stroke inflammation in female diabetic animals. C21 may be a useful therapeutic option to lower neuro-inflammation and improve the post-stroke recovery in diabetes. Full article
(This article belongs to the Special Issue The Renin Angiotensin System, Molecular, Geroscience and Aging-Related Disorders 2.0)
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Review

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23 pages, 1597 KiB  
Review
Role of the Renin–Angiotensin–Aldosterone System in Dystrophin-Deficient Cardiomyopathy
by Moises Rodriguez-Gonzalez, Manuel Lubian-Gutierrez, Helena Maria Cascales-Poyatos, Alvaro Antonio Perez-Reviriego and Ana Castellano-Martinez
Int. J. Mol. Sci. 2021, 22(1), 356; https://doi.org/10.3390/ijms22010356 - 31 Dec 2020
Cited by 5 | Viewed by 2825
Abstract
Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the [...] Read more.
Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin–angiotensin–aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Additionally, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration. Full article
(This article belongs to the Special Issue The Renin Angiotensin System, Molecular, Geroscience and Aging-Related Disorders 2.0)
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