Leukotrienes biosynthesis in coronary artery disease - results of Leukotrienes and Thromboxane In Myocardial Infarction (LTIMI) study

Stodółkiewicz, Edyta; Rewerska, Barbara; Rzeszutko, Marcin; Tomala, Marek; Chrustowicz, Anton; Żmudka, Krzysztof; Sanak, Marek; Szczeklik, Wojciech

doi:10.20452/pamw.4140

Cited by 3 publications

(1 citation statement)

References 14 publications

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“…This effect of MK can be attributed to its anti-inflammatory and antioxidant effects [88]. A single-center, prospective, observational study showed that patients with previous myocardial infarction had higher urinary LTs as compared with unstable angina [89].…”

Section: Montelukast and Myocardial Infarctionmentioning

confidence: 99%

Montelukast and Acute Coronary Syndrome: The Endowed Drug

et al. 2022

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Acute coronary syndrome (ACS) is a set of signs and symptoms caused by a reduction of coronary blood flow with subsequent myocardial ischemia. ACS is associated with activation of the leukotriene (LT) pathway with subsequent releases of various LTs, including LTB4, LTC4, and LTD4, which cause inflammatory changes and induction of immunothrombosis. LTs through cysteine leukotriene (CysLT) induce activation of platelets and clotting factors with succeeding coronary thrombosis. CysLT receptor (CysLTR) antagonists such as montelukast (MK) may reduce the risk of the development of ACS and associated complications through suppression of the activation of platelet and clotting factors. Thus, this critical review aimed to elucidate the possible protective role of MK in the management of ACS. The LT pathway is implicated in the pathogenesis of atherosclerosis, cardiac hypertrophy, and heart failure. Inhibition of the LT pathway and CysL1TR by MK might be effective in preventing cardiovascular complications. MK could be an effective novel therapy in the management of ACS through inhibition of pro-inflammatory CysLT1R and modulation of inflammatory signaling pathways. MK can attenuate thrombotic events by inhibiting platelet activation and clotting factors that are activated during the development of ACS. In conclusion, MK could be an effective agent in reducing the severity of ACS and associated complications. Experimental, preclinical, and clinical studies are recommended to confirm the potential therapeutic of MK in the management of ACS.

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Section: Montelukast and Myocardial Infarctionmentioning

confidence: 99%

Montelukast and Acute Coronary Syndrome: The Endowed Drug

et al. 2022

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A UHPLC-Q-TOF-MS-based serum and urine metabolomics approach reveals the mechanism of Gualou-Xiebai herb pair intervention against atherosclerosis process in ApoE-/- mice

Wang

Sun

Qiu

et al. 2023

Journal of Chromatography B

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Arachidonate 5-lipoxygenase is essential for biosynthesis of specialized pro-resolving mediators and cardiac repair in heart failure

Halade

Kain

Hossain

et al. 2022

American Journal of Physiology-Heart and Circulatory Physiology

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Arachidonate 5 lipoxygenase-derived leukotrienes are primary signals of leukocyte activation and inflammation in response to ischemic cardiac injury (MI; myocardial infarction). Using risk-free male C57BL/6J and arachidonate 5-lipoxygenase (ALOX5) null mice (8-12 weeks), we quantitated leukocytes and ALOX5-derived bioactive lipids of the infarcted left ventricle (LV) and spleen to measure the physiological inflammation and cardiac repair. Our results showed that ALOX5 endogenously generates specialized pro-resolving mediators (SPMs) that facilitate cardiac repair post-MI. Deficiency of ALOX5 lead to increase cyclooxygenase gene expression, 6-keto prostaglandin F1α, and neutrophil abundance with signs of unresolved inflammation post-MI. Consequently, ALOX5 deficiency impaired the resolution of inflammation and cardiac repair, including increased myocardium rupture post-MI in acute heart failure. On-time ALOX5 activation is critical for leukocyte abundance from the infarcted heart, indicating an essential role of ALOX5 in the resolution of inflammation. In addition, to balance the inflammatory responses, ALOX5 is also necessary for fibroblast signaling, as the ALOX5-deficient fibroblast are prone to fibroblast-to-myofibroblast differentiation leading to defective scar formation in post-MI cardiac repair. Consistent with these findings, ALOX5-null mice showed an overly inflammatory response, defective fibrotic signaling, and unresolved inflammation. These findings are indicative of a critical role of ALOX5 in myocardium healing, inflammation-resolution signaling, cardiac repair, and fibroblast pathophysiology.

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Leukotrienes biosynthesis in coronary artery disease - results of Leukotrienes and Thromboxane In Myocardial Infarction (LTIMI) study

Cited by 3 publications

References 14 publications

Montelukast and Acute Coronary Syndrome: The Endowed Drug

Montelukast and Acute Coronary Syndrome: The Endowed Drug

A UHPLC-Q-TOF-MS-based serum and urine metabolomics approach reveals the mechanism of Gualou-Xiebai herb pair intervention against atherosclerosis process in ApoE-/- mice

Arachidonate 5-lipoxygenase is essential for biosynthesis of specialized pro-resolving mediators and cardiac repair in heart failure

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