Preconditioning or Postconditioning with 8-Br-cAMP-AM Protects the Heart against Regional Ischemia and Reperfusion: A Role for Mitochondrial Permeability Transition

Khaliulin, Igor; Ascione, Raimondo; Маслов, Л Н; Amal, Haitham; Suleiman, M‐Saadeh

doi:10.3390/cells10051223

Cited by 13 publications

(11 citation statements)

References 78 publications

(91 reference statements)

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“…It has been demonstrated that IP limits the infarct size, and attenuates necrosis, apoptosis as well as cardiac dysfunction due to I/R injury [ 98 , 99 , 100 , 101 , 102 , 103 ]. These beneficial effects of IP are reported to be mediated through the activation of adenosine receptors [ 99 ] and protein kinase C activity [ 101 , 104 , 105 , 106 , 107 ], as well as due to reduced phospholipase activities [ 108 ] and the attenuation of TNF-α levels [ 109 ].…”

Section: Subcellular Modification Due To Ischemic Preconditioningmentioning

confidence: 99%

Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning

Tappia

Shah

Ramjiawan

et al. 2022

IJMS

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It is now well established that ischemia/reperfusion (I/R) injury is associated with the compromised recovery of cardiac contractile function. Such an adverse effect of I/R injury in the heart is attributed to the development of oxidative stress and intracellular Ca2+-overload, which are known to induce remodeling of subcellular organelles such as sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils. However, repeated episodes of brief periods of ischemia followed by reperfusion or ischemic preconditioning (IP) have been shown to improve cardiac function and exert cardioprotective actions against the adverse effects of prolonged I/R injury. This protective action of IP in attenuating myocardial damage and subcellular remodeling is likely to be due to marked reductions in the occurrence of oxidative stress and intracellular Ca2+-overload in cardiomyocytes. In addition, the beneficial actions of IP have been attributed to the depression of proteolytic activities and inflammatory levels of cytokines as well as the activation of the nuclear factor erythroid factor 2-mediated signal transduction pathway. Accordingly, this review is intended to describe some of the changes in subcellular organelles, which are induced in cardiomyocytes by I/R for the occurrence of oxidative stress and intracellular Ca2+-overload and highlight some of the mechanisms for explaining the cardioprotective effects of IP.

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Section: Subcellular Modification Due To Ischemic Preconditioningmentioning

confidence: 99%

Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning

Tappia

Shah

Ramjiawan

et al. 2022

IJMS

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“…HK2 is also a well-known regulator of mPTP opening. Accordingly, the cell-permeable cAMP analog 8-Br has recently been shown to protect the heart against regional I/R injury at the onset of reperfusion by promoting the binding of HK2 to mitochondria and inhibiting mPTP, as measured by the reduction in Ca 2+ -induced mitochondria swelling [237]. This study contrasts with the one reported by Pereira et al (2020), in which in vitro dissociation of mt-HK2 from mitochondria has no effect on mPTP opening in postconditioned hearts [120].…”

Section: Pyroptosismentioning

confidence: 99%

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

García-Niño

Zazueta

Buelna‐Chontal

et al. 2021

Life

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Mitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury by activating protective signaling pathways that prevent the exacerbated production of reactive oxygen/nitrogen species, inhibit opening of mitochondrial permeability transition pore and reduce apoptosis, maintaining normal mitochondrial function. Cardioprotection also involves the activation of mitochondrial quality control (MQC) processes, which replace defective mitochondria or eliminate mitochondrial debris, preserving the structure and function of the network of these organelles, and consequently ensuring homeostasis and survival of cardiomyocytes. Such processes include mitochondrial biogenesis, fission, fusion, mitophagy and mitochondrial-controlled cell death. This review updates recent advances in MQC mechanisms that are activated in the protection conferred by different cardiac conditioning interventions. Furthermore, the role of extracellular vesicles in mitochondrial protection and turnover of these organelles will be discussed. It is concluded that modulation of MQC mechanisms and recognition of mitochondrial targets could provide a potential and selective therapeutic approach for I/R-induced mitochondrial dysfunction.

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“…Acute myocardial infarction remains one of the most significant causes of death and post-event functional disability in population throughout the world [1]. In the circumstances the myocardium is deprived of blood that leads to an acute mass death of its cells and as a consequence results in the loss of cardiac contractility, collagen scar formation and subsequent progressing remodeling as well as heart insufficiency [2].…”

Section: Introductionmentioning

confidence: 99%

cAMP сoncentrations in cardiac mitochondria and serum in the С57ВL/6 mice under independent melanoma В16/F10 growth versus melanoma В16/F10 growth linked to chronic neurogenic pain

Frantsiyants¹,

Bandovkina²,

Neskubina³

et al. 2022

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The aim of this research work is to study the cAMP level in the cardiac mitochondria and serum in the С57ВL/6 strain mice of both genders under the independent melanoma В16/F10 growth versus the melanoma В16/F10 growth linked to chronic neurogenic pain (CNP). Materials and methods. Mice of strain С57ВL/6 (n=336) have been grouped as follows: the intact group of the mice (♂n=21; ♀n=21), the reference group (♂n=21; ♀n=21) with the reproduced CNP model, the comparison group (♂n=63; ♀n=63) to include the mice with melanoma В16/F10, and the main test group (♂n=63; ♀n=63) to cover the mice with the melanoma growth against the CNP background. Upon expiration of 1 week, 2 and 3 weeks of the melanoma growth, in the animals of the above experimental groups the cardiac mitochondria have been isolated with the centrifugation using high-performance refrigerated centrifuge Avanti J-E, BECMAN COULTER, USA. With ELISA Kit (RayBio USA) we have determined cAMP concentrations in serum and in the cardiac mitochondria. Results. CNP has induced a decrease in the cAMP level in the cardiac mitochondria by a factor of 3,6 in the female mice only. In the animals of the comparison group the cAMP level in the heart has been increasing beginning with week 2 of the tumor growth on average by a factor of 4, while in the main test group starting from week 1 of the tumor growth it has been recorded 2-4 times higher and was depleted by the end of the experiment. As to the cAMP concentration in serum, the dynamics thereof has not been found to be in correlation with the cardiac mitochondrial data, and its concentration decrease has been recorded both in the females and the males. Conclusion. So, the changes in the cAMP concentration in the cardiac mitochondria demonstrate their gender-specific feature; the female mice as against the males have responded to an independent impact produced by CNP. As to the main test group, CNP has stimulated an increase in the cAMP level in the cardiac mitochondria 1 week earlier than it is the case with the comparison group, and it has resulted in the full cAMP depletion by the 3rd week of the experiment.

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Preconditioning or Postconditioning with 8-Br-cAMP-AM Protects the Heart against Regional Ischemia and Reperfusion: A Role for Mitochondrial Permeability Transition

Cited by 13 publications

References 78 publications

Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning

Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

cAMP сoncentrations in cardiac mitochondria and serum in the С57ВL/6 mice under independent melanoma В16/F10 growth versus melanoma В16/F10 growth linked to chronic neurogenic pain

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