MicroRNA 21 Inhibits Left Ventricular Remodeling in the Early Phase of Rat Model with Ischemia-reperfusion Injury by Suppressing Cell Apoptosis

The significant reduction in ‘ischemic time’ through capillary diffusion of primary percutaneous intervention (pPCI) has rendered myocardial-ischemia reperfusion injury (MIRI) prevention a major issue in order to improve the prognosis of ST elevation myocardial infarction (STEMI) patients. In fact, while the ischemic damage increases with the severity and the duration of blood flow reduction, reperfusion injury reaches its maximum with a moderate amount of ischemic injury. MIRI leads to the development of post-STEMI left ventricular remodeling (post-STEMI LVR), thereby increasing the risk of arrhythmias and heart failure. Single pharmacological and mechanical interventions have shown some benefits, but have not satisfactorily reduced mortality. Therefore, a multitarget therapeutic strategy is needed, but no univocal indications have come from the clinical trials performed so far. On the basis of the results of the consistent clinical studies analyzed in this review, we try to design a randomized clinical trial aimed at evaluating the effects of a reasoned multitarget therapeutic strategy on the prevention of post-STEMI LVR. In fact, we believe that the correct timing of pharmacological and mechanical intervention application, according to their specific ability to interfere with survival pathways, may significantly reduce the incidence of post-STEMI LVR and thus improve patient prognosis.

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MicroRNA‑20b‑5p promotes ventricular remodeling by targeting the TGF‑β/Smad signaling pathway in a rat model of ischemia‑reperfusion injury

International Journal of Molecular Medicine ◽

10.3892/ijmm.2018.3695 ◽

2018 ◽

Cited By ~ 3

Author(s):

Zhao‑Guang Liang ◽

Hong Yao ◽

Rong‑Sheng Xie ◽

Chun‑Lin Gong ◽

Ye Tian

Keyword(s):

Reperfusion Injury ◽

Signaling Pathway ◽

Rat Model ◽

Ventricular Remodeling ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Smad Signaling ◽

Smad Signaling Pathway

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Pathophysiology, Diagnosis, and Management of Coronary No-Reflow Phenomenon

International Journal of Angiology ◽

10.1055/s-0041-1735949 ◽

2022 ◽

Author(s):

Gagan Kaur ◽

Patrick Baghdasaryan ◽

Balaji Natarajan ◽

Prabhdeep Sethi ◽

Ashis Mukherjee ◽

...

Keyword(s):

Ventricular Remodeling ◽

Ischemia Reperfusion Injury ◽

Left Ventricular Remodeling ◽

Ischemia Reperfusion ◽

Left Ventricular ◽

Clinical Predictors ◽

Catheterization Laboratory ◽

Cardiac Catheterization Laboratory ◽

No Reflow ◽

No Reflow Phenomenon

AbstractCoronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but they have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.

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Abstract 17348: Necrostatin 7 Limits Myocardial Infarct Size and Reduces Cardiac Remodeling After Permanent Coronary Occlusion in Rats

Circulation ◽

10.1161/circ.130.suppl_2.17348 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Yuri Dmitriev ◽

Sarkis Minasian ◽

Anna Dracheva ◽

Andrey Karpov ◽

Svetlana Chefu ◽

...

Keyword(s):

Infarct Size ◽

Rat Model ◽

Coronary Occlusion ◽

Ventricular Remodeling ◽

Ischemia Reperfusion Injury ◽

Myocardial Infarct ◽

Ischemia Reperfusion ◽

Morphological Characteristics ◽

Left Ventricular ◽

Myocardial Infarct Size

Background: Reduction of irreversible myocardial ischemia-reperfusion injury (IRI) remains important. One of the promising strategies aimed at myocardial IRI alleviation is modulation of programmed cell death (PCD) pathways. PCD mode displaying morphological characteristics of necrosis, and amenable to pharmacological manipulation is referred to as necroptosis. Necroptosis inhibitor necrostatin-1 has been shown to exert cardio- and neuroprotective effects. In the present work, the effect of necrostatin-7 (Nec-7) on myocardial injury in the rat model of permanent coronary occlusion was studied. Methods: Male Wistar rats (n = 19) were anesthetized with pentobarbital. The animals were subjected to permanent coronary occlusion (PCO) and intraperitoneal (i.p.) Nec-7 administration 1 h prior to PCO at a dose of 14.5 mg/kg in dimethyl sulfoxide (DMSO) or DMSO alone at a dose of 3.1 g/kg. Control rats were treated with saline. Three weeks after PCO, serum levels of NT-proBNP were measured, and histological outcomes were assessed. The infarct size (IS, %) and infarct length (IL, mm) were analyzed morphometrically. Results: DMSO caused significant reduction in serum NT-proBNP level vs. Control (0.3 ± 0.19 vs. 0.5 ± 0.22 ng/ml, p = 0.001), while Nec-7 further decreased NT-proBNP level in comparison with DMSO (0.2 ± 0.14 ng/ml, p = 0.008 vs. DMSO). Compared with Control, DMSO reduced adverse left ventricular remodeling, as evidenced by reduction in IS (16.0 ± 2.92 and 12.9 ± 1.72%, p = 0.015) and IL (6.2 ± 0.89 and 3.8 ± 0.35 mm, p = 0.008). Nec-7 treatment resulted in additional reduction of both IS and IL vs. DMSO group (9.0 ± 4.91 % and 2.9 ± 1.62 mm, respectively; p = 0.013 and p = 0.011 vs. DMSO, respectively). Conclusion: Nec-7 has cardioprotective properties, reducing myocardial wall stress and myocardial remodeling in the rat model of myocardial infarction.

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