Cellular Effects of Butyrate on Vascular Smooth Muscle Cells are Mediated through Disparate Actions on Dual Targets, Histone Deacetylase (HDAC) Activity and PI3K/Akt Signaling Network

Mathew, Omana P.; Ranganna, Kasturi; Mathew, Joseph; Zhu, Meiling; Yousefipour, Zivar; Selvam, Chelliah; Milton, Shirlette G.

doi:10.3390/ijms20122902

Cited by 34 publications

(23 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Saito et al found that Bacteroides fragilis ( B. fragilis ) is able to protect HT29 cells from apoptosis resulting from Shiga toxin [ 45 ]. Butyrate promotes vascular smooth muscle cell growth via proliferation arrest as well as apoptosis inhibition [ 46 ]. Notably, there are proapoptotic effects as well.…”

Section: Mechanisms Underlying the Interaction Between Gut Microbimentioning

confidence: 99%

Implication of Gut Microbiota in Cardiovascular Diseases

Zhou

Cheng

Zhu

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Emerging evidence has identified the association between gut microbiota and various diseases, including cardiovascular diseases (CVDs). Altered intestinal flora composition has been described in detail in CVDs, such as hypertension, atherosclerosis, myocardial infarction, heart failure, and arrhythmia. In contrast, the importance of fermentation metabolites, such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acid (BA), has also been implicated in CVD development, prevention, treatment, and prognosis. The potential mechanisms are conventionally thought to involve immune regulation, host energy metabolism, and oxidative stress. However, numerous types of programmed cell death, including apoptosis, autophagy, pyroptosis, ferroptosis, and clockophagy, also serve as a key link in microbiome-host cross talk. In this review, we introduced and summarized the results from recent studies dealing with the relationship between gut microbiota and cardiac disorders, highlighting the role of programmed cell death. We hope to shed light on microbiota-targeted therapeutic strategies in CVD management.

show abstract

Section: Mechanisms Underlying the Interaction Between Gut Microbimentioning

confidence: 99%

Implication of Gut Microbiota in Cardiovascular Diseases

Zhou

Cheng

Zhu

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“… 277 A recent study has demonstrated that butyrate inhibits proliferation via the HDAC and PI3K/Akt signaling network. 278 …”

Section: Main Textmentioning

confidence: 99%

Targeting the epigenome in in-stent restenosis: from mechanisms to therapy

Yang

Guo

et al. 2021

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

Coronary artery disease (CAD) is one of the most common causes of death worldwide. The introduction of percutaneous revascularization has revolutionized the therapy of patients with CAD. Despite the advent of drug-eluting stents, restenosis remains the main challenge in treating patients with CAD. In-stent restenosis (ISR) indicates the reduction in lumen diameter after percutaneous coronary intervention, in which the vessel’s lumen re-narrowing is attributed to the aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) and dysregulation of endothelial cells (ECs). Increasing evidence has demonstrated that epigenetics is involved in the occurrence and progression of ISR. In this review, we provide the latest and comprehensive analysis of three separate but related epigenetic mechanisms regulating ISR, namely, DNA methylation, histone modification, and non-coding RNAs. Initially, we discuss the mechanism of restenosis. Furthermore, we discuss the biological mechanism underlying the diverse epigenetic modifications modulating gene expression and functions of VSMCs, as well as ECs in ISR. Finally, we discuss potential therapeutic targets of the small molecule inhibitors of cardiovascular epigenetic factors. A more detailed understanding of epigenetic regulation is essential for elucidating this complex biological process, which will assist in developing and improving ISR therapy.

show abstract

“…The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signalling pathway, as well as the downstream targets of Akt, play a central role in several cellular processes, such as growth, proliferation, death and differentiation [ 100 , 101 ], and are also implicated in the regulation of vSMC proliferation and contractility. Insulin as well as insulin-like growth factor (IGF) signalling suppress the de-differentiation programme in vSMCs and maintain their contractile phenotype via the classical PI3K/Akt pathway [ 102 ].…”

Section: Signalling Pathways Implicated In Phenotypic Modulationmentioning

confidence: 99%

Phenotypic Modulation of Macrophages and Vascular Smooth Muscle Cells in Atherosclerosis—Nitro-Redox Interconnections

et al. 2021

View full text Add to dashboard Cite

Monocytes/macrophages and vascular smooth muscle cells (vSMCs) are the main cell types implicated in atherosclerosis development, and unlike other mature cell types, both retain a remarkable plasticity. In mature vessels, differentiated vSMCs control the vascular tone and the blood pressure. In response to vascular injury and modifications of the local environment (inflammation, oxidative stress), vSMCs switch from a contractile to a secretory phenotype and also display macrophagic markers expression and a macrophagic behaviour. Endothelial dysfunction promotes adhesion to the endothelium of monocytes, which infiltrate the sub-endothelium and differentiate into macrophages. The latter become polarised into M1 (pro-inflammatory), M2 (anti-inflammatory) or Mox macrophages (oxidative stress phenotype). Both monocyte-derived macrophages and macrophage-like vSMCs are able to internalise and accumulate oxLDL, leading to formation of “foam cells” within atherosclerotic plaques. Variations in the levels of nitric oxide (NO) can affect several of the molecular pathways implicated in the described phenomena. Elucidation of the underlying mechanisms could help to identify novel specific therapeutic targets, but to date much remains to be explored. The present article is an overview of the different factors and signalling pathways implicated in plaque formation and of the effects of NO on the molecular steps of the phenotypic switch of macrophages and vSMCs.

show abstract

Cellular Effects of Butyrate on Vascular Smooth Muscle Cells are Mediated through Disparate Actions on Dual Targets, Histone Deacetylase (HDAC) Activity and PI3K/Akt Signaling Network

Cited by 34 publications

References 75 publications

Implication of Gut Microbiota in Cardiovascular Diseases

Implication of Gut Microbiota in Cardiovascular Diseases

Targeting the epigenome in in-stent restenosis: from mechanisms to therapy

Phenotypic Modulation of Macrophages and Vascular Smooth Muscle Cells in Atherosclerosis—Nitro-Redox Interconnections

Contact Info

Product

Resources

About