Dynamic modulation of gut microbiota improves post‐myocardial infarct tissue repair in rats via butyric acid‐mediated histone deacetylase inhibition

Song, Tongtong; Guan, Xin Yuan; Wang, Xuan; Qu, Shanshan; Zhang, Siwei; Hui, Wenting; Men, Lihui; Chen, Xia

doi:10.1096/fj.201903129rrr

Cited by 20 publications

(11 citation statements)

References 42 publications

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“…Additionally, some studies reported that gut microbiota possibly affected the post-MI acetylation levels and tissue repair by influencing butyric acid production (Song et al, 2021). These results prove the role of HDAC4 inhibition in promoting CSC-derived cardiac regeneration and improving cardiac function recovery.…”

Section: Histone Modifications and Hdacs In MImentioning

confidence: 58%

Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics

Chen¹,

Liu²,

Ma³

et al. 2021

Front. Genet.

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Myocardial infarction (MI) is a complicated pathology triggered by numerous environmental and genetic factors. Understanding the effect of epigenetic regulation mechanisms on the cardiovascular disease would advance the field and promote prophylactic methods targeting epigenetic mechanisms. Genetic screening guides individualised MI therapies and surveillance. The present review reported the latest development on the epigenetic regulation of MI in terms of DNA methylation, histone modifications, and microRNA-dependent MI mechanisms and the novel therapies based on epigenetics.

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Section: Histone Modifications and Hdacs In MImentioning

confidence: 58%

Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics

Chen¹,

Liu²,

Ma³

et al. 2021

Front. Genet.

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“…Studies showed that a decrease in Akkermansia is related to obesity and diabetes, and the introduction of Akkermansia could reverse the metabolic disorder and improve inflammation in diabetics and obese patients [ 33 ]. However, studies have also shown that the increase in Streptococcaceae is significantly correlated with myocardial infarction [ 34 ]. After PFM-SR61-2 intervention, the beneficial bacteria Bifidobacteriaceae significantly displayed an increased abundance.…”

Section: Resultsmentioning

confidence: 99%

Antihypertensive Activity of Milk Fermented by Lactiplantibacillus plantarum SR37-3 and SR61-2 in L-NAME-Induced Hypertensive Rats

Yuan

Chen

et al. 2022

Foods

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Probiotic fermented milk can lower the incidence rate of hypertension and is beneficial to the regulation of the intestinal microecology. However, the underlying molecular mechanism remains elusive. Here, we evaluated the role of the gut microbiota and its metabolites in the antihypertensive effect of milk fermented by the Lactiplantibacillus plantarum strains SR37-3 (PFM-SR37-3) and SR61-2 (PFM-SR61-2) in Ng-nitro-L-arginine methyl ester induced hypertensive rats. The results showed that PFM-SR37-3 and PFM-SR61-2 intervention significantly lowered the blood pressure (BP) of NG-nitro-L-arginine methyl ester induced hypertensive rats and attenuated renal injury. In particular, long-term administration of PFM inhibited a progressive elevation in SBP (170.22 ± 8.40 and 133.28 ± 6.09 by model group and PFM-SR37-3 treated model group, respectively, at the end of the 4 weeks; p < 0.01 PFM-SR37-3 treated model group versus model group) and DBP (133.83 ± 5.91 and 103.00 ± 6.41 by model group and PFM-SR37-3 treated model group, respectively, at the end of the 4 weeks; p < 0.01 PFM-SR37-3 treated model group versus model group). PFM-SR37-3 and PFM-SR61-2 reshaped the gut microbiome and metabolome, and especially regulated the metabolic levels of L-phenylalanine, L-methionine and L-valine in the intestine and blood circulation. The analysis of the target organ’s aortic transcriptome indicated that the protective effects of PFM-SR37-3 and PFM-SR61-2 were accompanied by the modulation of the BP circadian rhythm pathway, which was conducive to cardiovascular function. Vascular transcriptomic analysis showed that circadian rhythm and AMPK might be potential targets of hypertension. In addition, the ACE inhibition rates of Lactiplantibacillus plantarum SR37-3 and Lactiplantibacillus plantarum SR61-2 in vitro were 70.5% and 68.9%, respectively. Our research provides new insights into novel and safe options for hypertension treatment.

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“…Butyric acid, a SCFA produced daily by gut microbiota, has been shown to benefit cardiovascular disease models. It has been reported that gut microbiota affected the acetylation level and tissue repair process after myocardial infarction by affecting the production of butyric acid ( 28 ). Previous studies have shown that butyrate intervention decreased potentially pathogenic species, including Desulfovibrionaceae , which was a potential group of endotoxin producers ( 29 , 30 ).…”

Section: Discussionmentioning

confidence: 99%

Butyric Acid Ameliorates Myocardial Fibrosis by Regulating M1/M2 Polarization of Macrophages and Promoting Recovery of Mitochondrial Function

You

et al. 2022

Front. Nutr.

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BackgroundWe aimed to investigate the effect and mechanism of butyric acid on rat myocardial fibrosis (MF).Methods16S rRNA sequencing was used to analyze the gut microbiota characteristics of the Sham group and MF group. HPLC was applied to measure butyric acid in the feces and serum. In vitro, rat macrophages RMa-bm were stimulated with LPS and IL-4, respectively, and then butyrate was added to study the influences of butyrate on M1/M2 polarization and mitochondrial function of rat macrophages. The rat macrophages and rat myocardial fibroblasts were co-cultured to explore the effect of butyrate on rat myocardial fibroblasts. In addition, MF rats were fed with butyric acid diet.ResultsCompared with the Sham group, collagen deposition in the MF group was increased, and fibrosis was serious. The abundance of Desulfovibrionaceae and Helicobacteraceae in the MF group was increased compared with the Sham group. Gut epithelial cells were destroyed in the MF group compared with the Sham group. Compared with the Sham group, LPS content in the MF group was increased and butyric acid was decreased. Butyrate inhibited M1 and promoted M2. Furthermore, butyrate may promote mitochondrial function recovery by regulating M1/M2 polarization of macrophages. After adding butyrate, cell proliferation ability was decreased, and aging and apoptosis were increased, which indicated that butyrate inhibited rat myocardial fibroblasts activity. Moreover, butyric acid could protect mitochondria and improve the symptoms of rats with MF.ConclusionsButyric acid ameliorated MF by regulating M1/M2 polarization of macrophages and promoting recovery of mitochondrial function.

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Dynamic modulation of gut microbiota improves post‐myocardial infarct tissue repair in rats via butyric acid‐mediated histone deacetylase inhibition

Cited by 20 publications

References 42 publications

Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics

Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics

Antihypertensive Activity of Milk Fermented by Lactiplantibacillus plantarum SR37-3 and SR61-2 in L-NAME-Induced Hypertensive Rats

Butyric Acid Ameliorates Myocardial Fibrosis by Regulating M1/M2 Polarization of Macrophages and Promoting Recovery of Mitochondrial Function

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