<scp>TGR</scp>5 activation induces cytoprotective changes in the heart and improves myocardial adaptability to physiologic, inotropic, and pressure‐induced stress in mice

Eblimit, Zeena; Thevananther, Sundararajah; Karpen, Saul J.; Taegtmeyer, Heinrich; Moore, David D.; Adorini, Luciano; Penny, Daniel J.; Desai, Moreshwar S.

doi:10.1111/1755-5922.12462

Cited by 58 publications

(49 citation statements)

References 52 publications

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“…31,32 More recently, they presented evidence that this isoform switch may be mediated by bile acids acting via a G-protein coupled receptor TGR5. 33 This intriguing line of inquiry needs further study.…”

Section: Discussionmentioning

confidence: 99%

Impaired myosin isoform shift and calcium transients contribute to cellular pathogenesis of rat cirrhotic cardiomyopathy

Honar

Liu

Zhang

et al. 2020

Liver International

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induced calcium release; dP/dT, Rate of rise of left ventricular pressure; dSL/ dt max , maximum velocities of shortening and relengthening; ECC, excitation-contraction coupling; E max , maximal cardiac elastance; FFR, force-frequency relation; FFT, fast fourier transformation; F max , maximum twitch force; F stst , steady-state twitch force; F tw , twitch force; I Ca,L , L-type Ca 2+ current; MHC, myosin heavy chain; PESP, post-extrasystolic potentiation; RMS SL , root mean square value of SL fluctuations; RyR, ryanodine receptor; SERCA, sarco/endoplasmic reticulum Ca 2+-ATPase; SL R , sarcomere length; SR, sarcoplasmic reticulum; t HR , time to half relaxation; t peak , time to peak shortening; TTP, time-to-peak Ca 2+ transient.

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Section: Discussionmentioning

confidence: 99%

Impaired myosin isoform shift and calcium transients contribute to cellular pathogenesis of rat cirrhotic cardiomyopathy

Honar

Liu

Zhang

et al. 2020

Liver International

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“…The presence of the TGR5 receptor in the heart has previously been demonstrated 6 . TGR5 activation has been reported to have cytoprotective effects in the mouse heart 21 . TGR5 belonged to G-protein-coupled receptor, also named as M-BAR, GPBAR1 or BG37, is an established target of bile acids.…”

Section: Discussionmentioning

confidence: 99%

TGR5 activation ameliorates hyperglycemia-induced cardiac hypertrophy in H9c2 cells

Cheng

Chang

Kuo

et al. 2019

Sci Rep

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Left ventricular hypertrophy is an independent risk factor in diabetic patients. TGR5 is shown to express in hearts, but its functional role in diabetes-induced cardiac hypertrophy remained unclear. The current study investigated the role of TGR5 on high glucose-induced hypertrophy of H9C2 cells. After incubation with a high level of glucose, H9C2 cells showed hypertrophic responses. Activation of TGR5 by lithocholic acid (LCA) ameliorated cell hypertrophy and enhanced SERCA2a and phosphorylated phospholamban (PLN) expression in H9C2 cells. Triamterene inhibited these effects at an effective dose to block TGR5. However, LCA failed to modify the free radical elevation induced by high-glucose in the H9c2 cells. Moreover, PKA inhibitors, but not an Epac blocker, markedly improved hyperglycemia-induced hypertrophy and attenuated the increased SERCA2a expression by LCA; it also attenuated the phosphorylated PLN and SERCA2a protein expression levels in high glucose-treated H9C2 cells. In conclusion, TGR5 activation stimulated protein kinase A (PKA) to enhance PLN phosphorylation, which activated SERCA2a to remove Ca 2+ from cytosol to sarcoplasmic reticulum in addition to the reduction of calcineurin/NFAT pathway signaling to ameliorate the hyperglycemia-induced cardiac hypertrophy shown in cardiomyocytes. TGR5 may service as a new target in the control of diabetic cardiomyopathy.

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“…A study showed that FXR and TGR5, which are expected to become the latest target of HF treatment, are closely related to inflammation, myocardial function, and hemodynamic stress [93,94].…”

Section: Imbalance Of Gut Microbe-derived Metabolitesmentioning

confidence: 99%

Cross‐Talk between Gut Microbiota and the Heart: A New Target for the Herbal Medicine Treatment of Heart Failure?

Zhong

Cheng

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Heart failure (HF) is the severe and terminal stage of various heart diseases. A growing number of studies have suggested the potential clinical significance of gut microbiota in the pathophysiology of HF. Herbal medicine (HM) plays a role in rebalancing the composition of gut microbiota and is widely used in the prevention and treatment of HF. There are many similarities between intestinal microecology and the traditional Chinese medicine (TCM) theory, such as the holistic concept and the theory of the “heart’s connection with the small intestine.” These similarities provide a theoretical basis for HM to prevent and treat diseases by regulating the intestinal flora and its metabolites. In this work, the cross-talk between gut microbiota and the heart is reviewed, and the relationship between TCM and gut microbiota is discussed. Based on the current literature and research, we hypothesize that the cross-talk between gut microbiota and the heart may offer a new therapeutic target for HF intervention.

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TGR5 activation induces cytoprotective changes in the heart and improves myocardial adaptability to physiologic, inotropic, and pressure‐induced stress in mice

Cited by 58 publications

References 52 publications

Impaired myosin isoform shift and calcium transients contribute to cellular pathogenesis of rat cirrhotic cardiomyopathy

Impaired myosin isoform shift and calcium transients contribute to cellular pathogenesis of rat cirrhotic cardiomyopathy

TGR5 activation ameliorates hyperglycemia-induced cardiac hypertrophy in H9c2 cells

Cross‐Talk between Gut Microbiota and the Heart: A New Target for the Herbal Medicine Treatment of Heart Failure?

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