Purpose of review This review aims to highlight the association between gut microbiome and cardiovascular disease (CVD) with emphasis on the possible molecular mechanisms by which how gut microbiome contributes to CVD. Recent findings Increasingly, the roles of gut microbiome in cardiovascular health and disease have gained much attention. Most of the investigations focus on how the gut dysbiosis contributes to CVD risk factors and which gut microbial-derived metabolites mediate such effects. Summary In this review, we discuss the molecular mechanisms of gut microbiome contributing to CVD, which include gut microbes translocalization to aortic artery because of gut barrier defect to initiate inflammation and microbial-derived metabolites inducing inflammation-signaling pathway and renal insufficiency. Specifically, we categorize beneficial and deleterious microbial-derived metabolites in cardiovascular health. We also summarize recent findings in the gut microbiome modulation of drug efficacy in treatment of CVD and the microbiome mechanisms by which how physical exercise ameliorates cardiovascular health. Gut microbiome has become an essential component of cardiovascular research and a crucial consideration factor in cardiovascular health and disease.

Gut microbiome and cardiovascular disease.

Cytochrome c can be released into extracellular space and modulate functions of human astrocytes in a toll-like receptor 4-dependent manner

Cardiovascular diseases (CVDs) are the result of complex pathophysiological processes in the tissues comprising the heart and blood vessels. Inflammation is the main culprit for the development of cardiovascular dysfunction, and it may be traced to cellular stress events including apoptosis, oxidative and shear stress, and cellular and humoral immune responses, all of which impair the system's structure and function. An intracellular chaperone, heat shock protein 60 (HSP60) is an intriguing example of a protein that may both be an ally and a foe for cardiovascular homeostasis; on one hand providing protection against cellular injury, and on the other triggering damaging responses through innate and adaptive immunity. In this review we will discuss the functions of HSP60 and its effects on cells and the immune system regulation, only to later address its implications in the development and progression of CVD. Lastly, we summarize the outcome of various studies targeting HSP60 as a potential therapeutic strategy for cardiovascular and other diseases.

Heat shock protein 60 and cardiovascular diseases: An intricate love-hate story.

Aim Intense interest remains in the identification of compounds to reduce human immunodeficiency virus type 1 (HIV-1) replication Coriolus versicolor’s polysaccharide peptide (PSP) has been demonstrated to possess immunomodulatory properties with the ability to activate an innate immune response through Toll-like receptor 4 (TLR4) showing insignificant toxicity This study sought to determine the potential use of PSP as an anti-HIV agent and whether its antiviral immune response was TLR4 dependent Materials and Methods HIV-1 p24 and anti-HIV chemokine release was assessed in HIV-positive (HIV+) THP1 cells and validated in HIV+ peripheral blood mononuclear cells (PBMCs), to determine PSP antiviral activity The involvement of TLR4 activation in PSP anti-HIV activity was evaluated by inhibition Results PSP showed a promising potential as an anti-HIV agent, by downregulating viral replication and promoting the upregulation of specific antiviral chemokines (RANTES, MIP-1α/β, and SDF-1α) known to block HIV-1 coreceptors in THP1 cells and human PBMCs PSP produced a 61% viral inhibition after PSP treatment in HIV-1-infected THP1 cells Additionally, PSP upregulated the expression of TLR4 and TLR4 inhibition led to countereffects in chemokine expression and HIV-1 replication Conclusion Taken together, these findings put forward the first evidence that PSP exerts an anti-HIV activity mediated by TLR4 and key antiviral chemokines Elucidating these new molecular mediators may reveal additional drug targets and open novel therapeutic avenues for HIV-1 infection

/pdf/naturally-derived-anti-hiv-polysaccharide-peptide-psp-33k5wbvoyu.pdf

Naturally Derived Anti-HIV Polysaccharide Peptide (PSP) Triggers a Toll-Like Receptor 4-Dependent Antiviral Immune Response.

Protective effect and mechanism of rebamipide on NSAIDs associated small bowel injury.

TAK-242 (resatorvid), a novel small-molecule cyclohexene derivative, inhibits TLR4 signaling selectively. TAK-242 blocked the Toll-like receptor (TLR) 4-triggered inflammatory signaling by binding directly to a specific amino acid Cys747 in the intracellular domain of TLR4. The present study was designed to examine the effects of TAK-242 on vascular inflammatory responses in human coronary artery endothelial cells (HCAECs) challenged by lipopolysaccharide (LPS, a TLR4 ligand). The results show that TAK-242 attenuated the LPS-induced expression of interleukin (IL)-6, IL-8 and monocyte chemoattractant protein 1 both at the transcription and translation levels in HCAECs. LPS-induced endothelial cell adhesion molecules, intercellular adhesion molecular-1 and vascular cell adhesion molecule-1 expressions were also reduced by treatment with TAK-242. In addition, coincubation with TAK-242 did not effect the expression of TLR4 in LPS-activated HCAECs. Furthermore, TAK-242 efficiently suppressed LPS-induced phosphorylation of nuclear factor κB (NF-κB) and IL-1 associated kinase-1 (IRAK-1) in HCAECs. These findings show that TAK-242 can suppress endothelial cell inflammation, suggesting that TAK-242 might be suitable for development as a therapeutic agent for inflammatory cardiovascular disease.

TAK-242 suppresses lipopolysaccharide-induced inflammation in human coronary artery endothelial cells.

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TAK-242 suppresses lipopolysaccharide-induced inflammation in human coronary artery endothelial cells.