The gut and cardiovascular diseases

ESC CardioMed ◽  
2018 ◽  
pp. 1090-1093
Author(s):  
Giuseppe Rosano

The physiological functioning of the gut is central for the pharmacokinetics of orally administered cardiovascular drugs and alteration of the gut homeostasis may have relevant repercussions on the effect of these drugs. The gut microbiome may affect the absorption and metabolism of nutrients favouring the development of obesity and diabetes. Furthermore, alterations in intestinal barrier permeability lead to the penetration of bacteria and bacterial wall products into the circulation and may contribute to the progression of atherosclerosis and worsening of heart failure. Despite the suggestions of the possible interaction between the gut and the cardiovascular system and of stimulating novel mechanisms for disease progression that may open to new therapeutic approaches, the available evidence must be considered preliminary.

2017 ◽  
Vol 89 (4) ◽  
pp. 91-94 ◽  
Author(s):  
A F Verbovoy ◽  
I A Tsanava ◽  
E V Mitroshina ◽  
L A Sharonova

Osteoprotegerin (OPG) is a glycoprotein that is a representative of the tumor necrosis factor-α receptor superfamily. Information about the possible role of OPG in the development of cardiovascular diseases has begun to appear in the literature in recent years. This review discusses the role of increasing the level of OPG in the development and progression of atherosclerosis and as a consequence of coronary heart disease and chronic heart failure.


2019 ◽  
Vol 317 (5) ◽  
pp. H923-H938 ◽  
Author(s):  
Adilah F. Ahmad ◽  
Girish Dwivedi ◽  
Fergal O’Gara ◽  
Jose Caparros-Martin ◽  
Natalie C. Ward

Cardiovascular disease (CVD) is the leading cause of death worldwide. The human body is populated by a diverse community of microbes, dominated by bacteria, but also including viruses and fungi. The largest and most complex of these communities is located in the gastrointestinal system and, with its associated genome, is known as the gut microbiome. Gut microbiome perturbations and related dysbiosis have been implicated in the progression and pathogenesis of CVD, including atherosclerosis, hypertension, and heart failure. Although there have been advances in the characterization and analysis of the gut microbiota and associated bacterial metabolites, the exact mechanisms through which they exert their action are not well understood. This review will focus on the role of the gut microbiome and associated functional components in the development and progression of atherosclerosis. Potential treatments to alter the gut microbiome to prevent or treat atherosclerosis and CVD are also discussed.


2020 ◽  
Vol 21 (12) ◽  
pp. 1264-1275
Author(s):  
Hongmin Sun ◽  
Lakshmi Pulakat ◽  
David W. Anderson

Chronic non-healing wounds are estimated to cost the US healthcare $28-$31 billion per year. Diabetic ulcers, arterial and venous ulcers, and pressure ulcers are some of the most common types of chronic wounds. The burden of chronic wounds continues to rise due to the current epidemic of obesity and diabetes and the increase in elderly adults in the population who are more vulnerable to chronic wounds than younger individuals. This patient population is also highly vulnerable to debilitating infections caused by opportunistic and multi-drug resistant pathogens. Reduced microcirculation, decreased availability of cytokines and growth factors that promote wound closure and healing, and infections by multi-drug resistant and biofilm forming microbes are some of the critical factors that contribute to the development of chronic non-healing wounds. This review discusses novel approaches to understand chronic wound pathology and methods to improve chronic wound care, particularly when chronic wounds are infected by multi-drug resistant, biofilm forming microbes.


2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
Rosalinda Sorrentino ◽  
Silvana Morello ◽  
Aldo Pinto

Cardiovascular diseases, formerly only attributed to the alterations of the stromal component, are now recognized as immune-based pathologies. Plasmacytoid Dendritic Cells (pDCs) are important immune orchestrators in heart and vessels. They highly produce IFN type I that promote the polarization of T cells towards a Th1 phenotype; however, pDCs can also participate to suppressive networks via the recruitment of T regulatory cells that downmodulate proinflammatory responses. pDCs populate the vessel wall layers during pathological conditions, such as atherosclerosis. It is thus clear that a better identification of pDCs activity in cardiovascular diseases can not only elucidate pathological mechanisms but also lead to new therapeutic approaches.


Circulation ◽  
2010 ◽  
Vol 121 (6) ◽  
pp. 822-830 ◽  
Author(s):  
Anne-Marie Lompré ◽  
Roger J. Hajjar ◽  
Sian E. Harding ◽  
Evangelia G. Kranias ◽  
Martin J. Lohse ◽  
...  

2021 ◽  
Vol 8 (9) ◽  
pp. 103
Author(s):  
Maryam Mahjoubin-Tehran ◽  
Stephen L. Atkin ◽  
Evgeny E. Bezsonov ◽  
Tannaz Jamialahmadi ◽  
Amirhossein Sahebkar

Cardiovascular disease (CVD) is the main cause of global death, highlighting the fact that conventional therapeutic approaches for the treatment of CVD patients are insufficient, and there is a need to develop new therapeutic approaches. In recent years, decoy technology, decoy oligodeoxynucleotides (ODN), and decoy peptides show promising results for the future treatment of CVDs. Decoy ODN inhibits transcription by binding to the transcriptional factor, while decoy peptide neutralizes receptors by binding to the ligands. This review focused on studies that have investigated the effects of decoy ODN and decoy peptides on non-atherosclerotic CVD.


2021 ◽  
Vol 22 (14) ◽  
pp. 7392
Author(s):  
Natthaphat Siri-Angkul ◽  
Behzad Dadfar ◽  
Riya Jaleel ◽  
Jazna Naushad ◽  
Jaseela Parambathazhath ◽  
...  

The occurrence and prevalence of heart failure remain high in the United States as well as globally. One person dies every 30 seconds from heart disease. Recognizing the importance of heart failure, clinicians and scientists have sought better therapeutic strategies and even cures for end-stage heart failure. This exploration has resulted in many failed clinical trials testing novel classes of pharmaceutical drugs and even gene therapy. As a result, along the way, there have been paradigm shifts toward and away from differing therapeutic approaches. The continued prevalence of death from heart failure, however, clearly demonstrates that the heart is not simply a pump and instead forces us to consider the complexity of simplicity in the pathophysiology of heart failure and reinforces the need to discover new therapeutic approaches.


2020 ◽  
Vol 319 (6) ◽  
pp. H1227-H1233
Author(s):  
Caitlin V. Lewis ◽  
W. Robert Taylor

The gut microbiome and intestinal dysfunction have emerged as potential contributors to the development of cardiovascular disease (CVD). Alterations in gut microbiome are well documented in hypertension, atherosclerosis, and heart failure and have been investigated as a therapeutic target. However, a perhaps underappreciated but related role for intestinal barrier function has become evident. Increased intestinal permeability is observed in patients and mouse models of CVD. This increased intestinal permeability can enhance systemic inflammation, alter gut immune function, and has been demonstrated as predictive of adverse cardiovascular outcomes. The goal of this review is to examine the evidence supporting a role for intestinal barrier function in cardiovascular disease and its prospect as a novel therapeutic target. We outline key studies that have investigated intestinal permeability in hypertension, coronary artery disease, atherosclerosis, heart failure, and myocardial infarction. We highlight the central mechanisms involved in the breakdown of barrier function and look at emerging evidence for restored barrier function as a contributor to promising treatment strategies such as short chain fatty acid, probiotic, and renin angiotensin system-targeted therapeutics. Recent studies of more selective targeting of the intestinal barrier to improve disease outcomes are also examined. We suggest that although current data supporting a contribution of intestinal permeability to CVD pathogenesis are largely associative, it appears to be a promising avenue for further investigation. Additional studies of the mechanisms of barrier restoration in CVD and testing of intestinal barrier-targeted compounds will be required to confirm their potential as a new class of CVD therapeutic.


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