BCL2‑regulated apoptotic process in myocardial ischemia‑reperfusion injury (Review)

Korshunova, A Yu; Благонравов, М. Л.; Неборак, Е. В.; Syatkin, S. P.; Sklifasovskaya, A. P.; Semyatov, S M; Agostinelli, Enzo

doi:10.3892/ijmm.2020.4781

Cited by 65 publications

(31 citation statements)

References 169 publications

(267 reference statements)

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“…In addition, in some studies on other apoptotic factors and TBI, there was a significant enhancement in CSF apoptotic factors (14,15). Korshunova et al observed that Bcl-2 could regulate apoptotic factors in myocardial ischemia/reperfusion injury (16). However, these studies were different from our study in terms of protocols.…”

Section: Discussioncontrasting

confidence: 85%

Assessing the Effect of Intrathecal Dexmedetomidine on Cerebrospinal Fluid Levels of Apoptotic Factors: A Clinical Trial Study in Lumbar Disc Surgery

et al. 2021

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Background: Dexmedetomidine protective effects on apoptosis in the brain and peripheral organs have been reported in vivo and in vitro. Apoptotic factors of cerebrospinal fluid (CSF) may influence the prognosis of patients undergoing open discectomy surgery. Objectives: This study evaluated the effect of intrathecal dexmedetomidine administration on the CSF levels of apoptotic factors and clinical outcomes in patients undergoing lumbar discectomy. Methods: This clinical trial was conducted on patients undergoing open lumbar discectomy. Forty patients were randomly divided into control and dexmedetomidine groups. In the dexmedetomidine group, 0.1 μg/kg of dexmedetomidine was intrathecally injected after anesthesia induction. Patients’ hemodynamic status during surgery was recorded; additionally, their pain scores were recorded by the Numeric Rating Scale (NRS) in the recovery room. The levels of apoptotic factors including Bax/Bcl-2 and caspase-3 in the CSF were measured at the beginning and end of discectomy, and the results were compared between the two groups. Results: Of the 40 evaluated patients, the mean levels of caspase-3 in the intervention and control groups were 2.28 ± 0.35 and 2.34 ± 0.32 ng/mL before surgery and 2.56 ± 0.42 and 2.72 ± 0.39 ng/mL after surgery, respectively. The levels of Bax/Bcl-2 in the intervention and control groups were 1.01 ± 0.11 and 0.89 ± 0.07 before surgery and 1.28 ± 0.14 and 1.16 ± 0.19 after surgery, respectively. The levels of these two factors were not significantly different. However, the NRS scores were significantly lower in the dexmedetomidine group than in the control group. Conclusions: Intrathecal dexmedetomidine could significantly and safely reduce the NRS score in the intervention group but did not have any significant effect on the CSF levels of apoptotic factors before and after lumbar discectomy surgery.

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Section: Discussioncontrasting

confidence: 85%

Assessing the Effect of Intrathecal Dexmedetomidine on Cerebrospinal Fluid Levels of Apoptotic Factors: A Clinical Trial Study in Lumbar Disc Surgery

et al. 2021

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“…The Bcl-2 family is involved in the intrinsic pathway of apoptosis; it includes proapoptotic proteins (such as Bad, Bax or Bid) and antiapoptotic proteins (such as Bcl-2 and Bcl-XL). Bcl-2 is regulated by several signaling pathways and substances, including JAK2/STAT3, PI3K/AKT, MEK1/ERK1/2, PTEN, cardiac ankyrin repeat protein, eNOS, and miRs [ 45 ]. Bcl2 is the target gene of miR-503 [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways

Cai

Sun

et al. 2022

Oxidative Medicine and Cellular Longevity

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Acute myocardial infarction is a leading cause of death worldwide, while restoration of blood flow to previously ischemic myocardium may lead to ischemia/reperfusion (I/R) injury. Accumulated evidence shows that microRNAs play important roles in cardiovascular diseases. However, the potential role of microRNA-503 (miR-503) in myocardial I/R injury is little known. Thus, this study is aimed at determining whether and how miR-503 affects myocardial I/R injury in vivo and in vitro. A mouse model of myocardial I/R injury and H9c2 cell model of hypoxia/reoxygenation (H/R) injury were established. The postischemic cardiac miR-503 was downregulated in vivo and in vitro. Mechanistically, PI3K p85 and Bcl-2 are miR-503 targets. The post-ischemic cardiac PI3K p85 protein level was decreased in vivo. Agomir-503 treatment exacerbated H/R-induced injuries manifested as decreased cell viability, increased lactate dehydrogenase activity, and cell apoptosis. Agomir-503 treatment reduced cell viability under normoxia as well and reduced both PI3K p85 and Bcl-2 protein levels under either normoxia or H/R condition. It reduced phosphorylation of Stat3 (p-Stat3-Y705) and Akt (T450) in cells subjected to H/R. In contrast, Antagomir-503 treatment attenuated H/R injury and increased p-Stat3 (Y705) under normoxia and increased p-Akt (T450) under either normoxia or H/R condition. It is concluded that miR-503 exacerbated I/R injury via inactivation of PI3K/Akt and STAT3 pathways and may become a therapeutic target in preventing myocardial I/R injury.

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“…Numerous studies have demonstrated that apoptosis plays an important role in cardiomyocyte death and is proposed to contribute to nal infarct size [28,29]. A pivotal event in the initiation of apoptotic cell death is ERS [6].…”

Section: Discussionmentioning

confidence: 99%

Puerarin protects against myocardial ischemia/reperfusion injury by inhibiting endoplasmic reticulum stress and apoptosis via activating the AMPK/NRF2 pathway

Yang

Liu

Wang

et al. 2021

Preprint

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Objective Puerarin was reported to protect against myocardial ischemia/reperfusion (IR) injury. The current study aims to investigate the protective effects of puerarin against myocardial IR injury and the underlying mechanisms. Methods The hearts were subjected to the ligation of the left anterior descending coronary artery and reperfusion. Before reperfusion, pretreatment with puerarin (100 mg/kg), with or without the AMPK inhibitor Compound c (0.25 mg/kg). Myocardial infarct size, the serum creatine kinase-MB (CK-MB) activity, cardiac function, apoptotic cell death, and the endoplasmic reticulum stress, as well as activation of the AMPK/NRF2 pathway were observed. Results Treatment with puerarin significantly decreased the myocardial infarct size, the serum CK-MB activity and notably alleviated IR-induced cardiac dysfunction. Moreover, puerarin reduced myocardial IR-induced apoptotic cell death. In addition, puerarin inhibited myocardial IR-induced endoplasmic reticulum stress and activated the AMPK/NRF2 pathway. More importantly, the AMPK inhibitor Compound c prevented these puerarin-induced cardioprotective effects and activation of the AMPK/NRF2 pathway, as well as apoptosis and the endoplasmic reticulum stress activation. Conclusion Our results show that puerarin alleviates myocardial IR injury by inhibiting apoptosis and endoplasmic reticulum stress via the AMPK/NRF2 pathway.

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BCL2‑regulated apoptotic process in myocardial ischemia‑reperfusion injury (Review)

Cited by 65 publications

References 169 publications

Assessing the Effect of Intrathecal Dexmedetomidine on Cerebrospinal Fluid Levels of Apoptotic Factors: A Clinical Trial Study in Lumbar Disc Surgery

Assessing the Effect of Intrathecal Dexmedetomidine on Cerebrospinal Fluid Levels of Apoptotic Factors: A Clinical Trial Study in Lumbar Disc Surgery

MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways

Puerarin protects against myocardial ischemia/reperfusion injury by inhibiting endoplasmic reticulum stress and apoptosis via activating the AMPK/NRF2 pathway

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