Yiqi Huoxue preserves heart function by upregulating the Sigma‑1 receptor in rats with myocardial infarction

Lou, Lixia; Li, Chunhong; Wang, Jie; Wu, Aiming; Zhang, Ting; Ma, Zhe; Chai, Limin; Zhang, Dongmei; Zhao, Yizhou; Nie, Bo; Jin, Qiushuo; Chen, Huiyang; Liu, Wei Jing

doi:10.3892/etm.2021.10743

Cited by 6 publications

(5 citation statements)

References 35 publications

(52 reference statements)

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“…Mouse anti-IP 3 R monoclonal primary antibody IP 3 R2 (sc-398434) was purchased commercially (Santa Cruz Biotechnology, Santa Cruz, CA, United States) and used at a dilution of 1:50. The specificity of antibody sc-398434 has been previously verified using Western blot by Lou et al (2021) . IP 3 R antibodies have been extensively covered in previous studies ( Hattori et al, 2004 ; Ando et al, 2006 ; Uchida et al, 2010 ; Salvador and Egger, 2018 ).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of adenylyl cyclase 1 by ST034307 inhibits IP3-evoked changes in sino-atrial node beat rate

et al. 2022

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Atrial arrhythmias, such as atrial fibrillation (AF), are a major mortality risk and a leading cause of stroke. The IP3 signalling pathway has been proposed as an atrial-specific target for AF therapy, and atrial IP3 signalling has been linked to the activation of calcium sensitive adenylyl cyclases AC1 and AC8. We investigated the involvement of AC1 in the response of intact mouse atrial tissue and isolated guinea pig atrial and sino-atrial node (SAN) cells to the α-adrenoceptor agonist phenylephrine (PE) using the selective AC1 inhibitor ST034307. The maximum rate change of spontaneously beating mouse right atrial tissue exposed to PE was reduced from 14.5% to 8.2% (p = 0.005) in the presence of 1 μM ST034307, whereas the increase in tension generated in paced left atrial tissue in the presence of PE was not inhibited by ST034307 (Control = 14.2%, ST034307 = 16.3%; p > 0.05). Experiments were performed using isolated guinea pig atrial and SAN cells loaded with Fluo-5F-AM to record changes in calcium transients (CaT) generated by 10 μM PE in the presence and absence of 1 μM ST034307. ST034307 significantly reduced the beating rate of SAN cells (0.34-fold decrease; p = 0.003) but did not inhibit changes in CaT amplitude in response to PE in atrial cells. The results presented here demonstrate pharmacologically the involvement of AC1 in the downstream response of atrial pacemaker activity to α-adrenoreceptor stimulation and IP3R calcium release.

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Section: Methodsmentioning

confidence: 99%

Inhibition of adenylyl cyclase 1 by ST034307 inhibits IP3-evoked changes in sino-atrial node beat rate

et al. 2022

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“…However, exogenous H 2 S was observed to reduce mitochondrial apoptotic proteins, cytochrome c, mPTP opening, and MFN2 expression, which had a cardioprotective effect. Additionally, researchers discovered that the herbal formula Yiqi Huoxue reduced the Sigma-1 receptor (a chaperone protein on MAMs) and increased IP3R2 expression in infarcted rats, which helped prevent cardiomyocyte hypertrophy ( Lou et al, 2021 ). Another study reported that FeA was found to attenuate MAM alterations induced by high glucose and ameliorate cardiomyopathy in diabetic rats ( Salin Raj et al, 2023 ).…”

Section: Mitochondria-associated Endoplasmic Reticulum Membranes As P...mentioning

confidence: 99%

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Ding,

Liu,

Zhang

et al. 2024

Front. Pharmacol.

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Cardiovascular diseases (CVDs) are currently the leading cause of death worldwide. In 2022, the CVDs contributed to 19.8 million deaths globally, accounting for one-third of all global deaths. With an aging population and changing lifestyles, CVDs pose a major threat to human health. Mitochondria-associated endoplasmic reticulum membranes (MAMs) are communication platforms between cellular organelles and regulate cellular physiological functions, including apoptosis, autophagy, and programmed necrosis. Further research has shown that MAMs play a critical role in the pathogenesis of CVDs, including myocardial ischemia and reperfusion injury, heart failure, pulmonary hypertension, and coronary atherosclerosis. This suggests that MAMs could be an important therapeutic target for managing CVDs. The goal of this study is to summarize the protein complex of MAMs, discuss its role in the pathological mechanisms of CVDs in terms of its functions such as Ca2+ transport, apoptotic signaling, and lipid metabolism, and suggest the possibility of MAMs as a potential therapeutic approach.

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“…SIG1R ensures stable Ca 2+ signal transduction between the ER and mitochondria by maintaining IP3R stability ( Hayashi & Su, 2007 ). Upregulation of SIG1R in rats plays a role in maintaining cardiac function ( Lou et al, 2021 ). SIG1R inhibition accelerates autophagy in cardiomyocytes in oxidative stress conditions ( Ortíz-Rentería et al, 2018 ).…”

Section: Roles Of Mam-related Proteins In Cardioprotectionmentioning

confidence: 99%

“…SIG1R KO mouse showed mitochondrial dysfunction, morphological abnormalities, and cardiac remodeling, leading to systolic dysfunction ( Luan et al, 2021 ). Upregulated SIG1R can preserve heart function in rats with MI ( Lou et al, 2021 ). Another study showed that genetically or pharmacologically targeted activation of BECN1 improved MAMs in the heart during endotoxemia, suggesting that BECN1 may also be involved in cardiac protective processes.…”

Section: Roles Of Mam-related Proteins In Cardioprotectionmentioning

confidence: 99%

Compositions and Functions of Mitochondria-Associated Endoplasmic Reticulum Membranes and Their Contribution to Cardioprotection by Exercise Preconditioning

Cheng

Peng

2022

Front. Physiol.

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Mitochondria-associated endoplasmic reticulum membranes (MAMs) are important components of intracellular signaling and contribute to the regulation of intracellular Ca2+/lipid homeostasis, mitochondrial dynamics, autophagy/mitophagy, apoptosis, and inflammation. Multiple studies have shown that proteins located on MAMs mediate cardioprotection. Exercise preconditioning (EP) has been shown to protect the myocardium from adverse stimuli, but these mechanisms are still being explored. Recently, a growing body of evidence points to MAMs, suggesting that exercise or EP may be involved in cardioprotection by modulating proteins on MAMs and subsequently affecting MAMs. In this review, we summarize the latest findings on MAMs, analyzing the structure and function of MAMs and the role of MAM-related proteins in cardioprotection. We focused on the possible mechanisms by which exercise or EP can modulate the involvement of MAMs in cardioprotection. We found that EP may affect MAMs by regulating changes in MFN2, MFN1, AMPK, FUNDC1, BECN1, VDAC1, GRP75, IP3R, CYPD, GSK3β, AKT, NLRP3, GRP78, and LC3, thus playing a cardioprotective role. We also provided direction for future studies that may be of interest so that more in-depth studies can be conducted to elucidate the relationship between EP and cardioprotection.

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Yiqi Huoxue preserves heart function by upregulating the Sigma‑1 receptor in rats with myocardial infarction

Cited by 6 publications

References 35 publications

Inhibition of adenylyl cyclase 1 by ST034307 inhibits IP3-evoked changes in sino-atrial node beat rate

Inhibition of adenylyl cyclase 1 by ST034307 inhibits IP3-evoked changes in sino-atrial node beat rate

Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases

Compositions and Functions of Mitochondria-Associated Endoplasmic Reticulum Membranes and Their Contribution to Cardioprotection by Exercise Preconditioning

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