Tubeimoside I Antagonizes Yoda1-Evoked Piezo1 Channel Activation

Liu, Silin; Pan, Xiaobo; Cheng, Wei; Deng, Bo; He, Yu; Zhang, Lei; Ning, Yile; Li, Jing

doi:10.3389/fphar.2020.00768

Cited by 31 publications

(21 citation statements)

References 36 publications

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“…Jedi1/2 is a new type of hydrophilic Piezo1 chemical activator, which acts through the peripheral blades and uses a peripheral lever-like device composed of blades and light beams to gate the central ion conduction hole ( 142 ). Recently, an analogue of Yoda1, named Dooku1 ( 147 ), and tubeimoside I (TBMS1) identified in traditional Chinese medicine ( 148 ), reversibly antagonizes the activation of Piezo1 induced by Yoda1 through competition for specific channel binding sites.…”

Section: Pharmacology and Physical Regulation Of Piezo1 Channelmentioning

confidence: 99%

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Liu

Zheng

et al. 2022

Front. Immunol.

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Mechanical damage is one of the predisposing factors of inflammation, and it runs through the entire inflammatory pathological process. Repeated or persistent damaging mechanical irritation leads to chronic inflammatory diseases. The mechanism of how mechanical forces induce inflammation is not fully understood. Piezo1 is a newly discovered mechanically sensitive ion channel. The Piezo1 channel opens in response to mechanical stimuli, transducing mechanical signals into an inflammatory cascade in the cell leading to tissue inflammation. A large amount of evidence shows that Piezo1 plays a vital role in the occurrence and progression of chronic inflammatory diseases. This mini-review briefly presents new evidence that Piezo1 responds to different mechanical stresses to trigger inflammation in various tissues. The discovery of Piezo1 provides new insights for the treatment of chronic inflammatory diseases related to mechanical stress. Inhibiting the transduction of damaging mechanical signals into inflammatory signals can inhibit inflammation and improve the outcome of inflammation at an early stage. The pharmacology of Piezo1 has shown bright prospects. The development of tissue-specific Piezo1 drugs for clinical use may be a new target for treating chronic inflammation.

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Section: Pharmacology and Physical Regulation Of Piezo1 Channelmentioning

confidence: 99%

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Liu

Zheng

et al. 2022

Front. Immunol.

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“…RR If administered from extracellular side, inhibits the inward rather than outward current of mPiezo1/2 alone, suggesting its pore-inhibiting mechanism 45 . Recent studies reported the recognition of other molecules, including Yoda1 analog named Dooku1 172 and the most recent compound Tubeimoside1 (TBMS1) extracted from Bolbostemma 173 , both with reversible antagonizing capability of Yoda1-evoked Piezo1 trigger (Table 3 ). They were reported to exert their effect through selective binding site competition with Yoda1.…”

Section: Piezo1 Pharmacologymentioning

confidence: 99%

Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target

Shinge¹,

Zhang²,

Din³

et al. 2022

Int. J. Biol. Sci.

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Purpose of Review: Atherosclerosis is the principal cause of cardiovascular diseases (CVDs) which are the major cause of death worldwide. Mechanical force plays an essential role in cardiovascular health and disease. To bring the awareness of mechanosensitive Piezo1 role in atherosclerosis and its therapeutic potentials we review recent literature to highlight its involvement in various mechanisms of the disease. Recent Findings: Recent studies reported Piezo1 channel as a sensor, and transducer of various mechanical forces into biochemical signals, which affect various cellular activities such as proliferation, migration, apoptosis and vascular remodeling including immune/inflammatory mechanisms fundamental phenomenon in atherogenesis. Summary: Numerous evidences suggest Piezo1 as a player in different mechanisms of cell biology, including immune/inflammatory and other cellular mechanisms correlated with atherosclerosis. This review discusses mechanistic insight about this matter and highlights the drugability and therapeutic potentials consistent with emerging functions Piezo1 in various mechanisms of atherosclerosis. Based on the recent works, we suggest Piezo1 as potential therapeutic target and a valid candidate for future research. Therefore, a deeper exploration of Piezo1 biology and translation towards the clinic will be a novel strategy for treating atherosclerosis and other CVDs.

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“…In our study, we found that IR decreased expression of SIRT1, but TBM could not reverse expression of SIRT1 (Figure S5 ). Recently, TBM has been reported to antagonize Yoda1-evoked Piezo1 channel activation [ 63 ]. Also, Piezo1 is proposed to be a vital factor that leads to cerebral ischemia-reperfusion injury [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Tubeimoside I Ameliorates Myocardial Ischemia‐Reperfusion Injury through SIRT3‐Dependent Regulation of Oxidative Stress and Apoptosis

Luo

Cheng

et al. 2021

Oxidative Medicine and Cellular Longevity

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Myocardial ischemia-reperfusion injury (MIRI) is a phenomenon that reperfusion leads to irreversible damage to the myocardium and increases mortality in acute myocardial infarction (AMI) patients. There is no effective drug to treat MIRI. Tubeimoside I (TBM) is a triterpenoid saponin purified from Chinese traditional medicine tubeimu. In this study, 4 mg/kg TBM was given to mice intraperitoneally at 15 min after ischemia. And TBM treatment improved postischemic cardiac function, decreased infarct size, diminished lactate dehydrogenase release, ameliorated oxidative stress, and reduced apoptotic index. Notably, ischemia-reperfusion induced a significant decrease in cardiac SIRT3 expression and activity, while TBM treatment upregulated SIRT3’s expression and activity. However, the cardioprotective effects of TBM were largely abolished by a SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP). This suggests that SIRT3 plays an essential role in TBM’s cardioprotective effects. In vitro, TBM also protected H9c2 cells against simulated ischemia/reperfusion (SIR) injury by attenuating oxidative stress and apoptosis, and siSIRT3 diminished its protective effects. Taken together, our results demonstrate for the first time that TBM protects against MIRI through SIRT3-dependent regulation of oxidative stress and apoptosis. TBM might be a potential drug candidate for MIRI treatment.

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Tubeimoside I Antagonizes Yoda1-Evoked Piezo1 Channel Activation

Cited by 31 publications

References 36 publications

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Emerging Piezo1 signaling in inflammation and atherosclerosis; a potential therapeutic target

Tubeimoside I Ameliorates Myocardial Ischemia‐Reperfusion Injury through SIRT3‐Dependent Regulation of Oxidative Stress and Apoptosis

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