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Cross talking between AMP activated protein kinase (AMPK) and innate immuno responses in heart tissue after myocardial ischemia
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Maryam Rameshrad   , Alireza Garjani , Nasrin Maleki Dizaji , Hamid Soraya , Bahador Bagheri , Haleh Vaez , Sina Andalib , Mojtaba Ziaee , Arash Khorrami |
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Abstract: (257 Views) |
Introduction: 5’-AMP-activated protein kinase (AMPK) as a sensor of energy in cells, is activated when nutrient supply and adenosine triphosphate (ATP) generation are limited or cellular energy demand is increased. The role of AMPK is particularly prominent in the heart, which has a high demand for energy in the form of ATP and little energy reserves. The function of AMPK is particularly important during low-energy states such as cardiac ischemia. Thus, AMPK is considered as a promising target for the protection of the heart from ischemic injury, cardiac hypertrophy, and heart failure.Toll-like receptors (TLRs) are found on cell surfaces or intracellular compartments. TLRs are the first line of the immune system and are mainly expressed on macrophages and dendritic cells for investigation of pathogenous micro-organisms. However, they also play an important role in many pathophysiological processes in human disease that do not involve pathogens. TLRs are also activated by damage-associated molecular patterns (DAMPs) which are released in response to tissue injury. Furthermore, not only classic immune cells but also non-bone marrow-derived cells take part in the inflammatory cascade through TLR signaling. Antigen-presenting cells and several types of parenchymal cells, including cardiomyocytes, also express TLRs.
Search Method: A review of the golden results of our previous studies.
Results: Our previous studies demonstrated that activating AMPK with metformin or A-769662 could block activated TLR-4 expression in the heart in conditions associated with inflammation such as myocardial infarction or septicemia. Furthermore, based on our in vivo and in vitro studies, coadministration of compound C as an AMPK inhibitor reversed the suppressive effects of AMPK activators on TLR4 expression and its downstream inflammatory pathway.
Conclusion: Collectively, these results indicate a clear link between AMPK and TLR4.
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| Keywords: AMPK, TLR4, myocardium, Inflammation |
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Full-Text [PDF 324 kb]
(39 Downloads)
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Type of Study: Research |
Subject:
General
Received: 2023/12/25 | Accepted: 2023/08/23 | Published: 2023/08/23
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