Targeting angiogenesis in myocardial infarction: Novel therapeutics (Review)

Li, Jiejie; Zhao, Yuanyuan; Zhu, Wei

doi:10.3892/etm.2021.10986

Cited by 24 publications

(17 citation statements)

References 116 publications

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“…The outcome is gradual decrease in the blood supply, which hinders oxygen supply, nutrients, and elimination of metabolic waste, promoting CM necrosis. Therefore, for cardiac regeneration in addition to functional CMs, reconstruction of vascular architecture is also essential to restore cardiac function [ 124 , 125 ]. Hence, therapeutic approaches that can promote endogenous vascularization in situ are noteworthy.…”

Section: Pc Reprogramming Into Induced Vascular Smcsmentioning

confidence: 99%

Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration

Perveen

Vanni

Iacono

et al. 2023

Cells

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Cardiac diseases are the foremost cause of morbidity and mortality worldwide. The heart has limited regenerative potential; therefore, lost cardiac tissue cannot be replenished after cardiac injury. Conventional therapies are unable to restore functional cardiac tissue. In recent decades, much attention has been paid to regenerative medicine to overcome this issue. Direct reprogramming is a promising therapeutic approach in regenerative cardiac medicine that has the potential to provide in situ cardiac regeneration. It consists of direct cell fate conversion of one cell type into another, avoiding transition through an intermediary pluripotent state. In injured cardiac tissue, this strategy directs transdifferentiation of resident non-myocyte cells (NMCs) into mature functional cardiac cells that help to restore the native tissue. Over the years, developments in reprogramming methods have suggested that regulation of several intrinsic factors in NMCs can help to achieve in situ direct cardiac reprogramming. Among NMCs, endogenous cardiac fibroblasts have been studied for their potential to be directly reprogrammed into both induced cardiomyocytes and induced cardiac progenitor cells, while pericytes can transdifferentiate towards endothelial cells and smooth muscle cells. This strategy has been indicated to improve heart function and reduce fibrosis after cardiac injury in preclinical models. This review summarizes the recent updates and progress in direct cardiac reprogramming of resident NMCs for in situ cardiac regeneration.

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Section: Pc Reprogramming Into Induced Vascular Smcsmentioning

confidence: 99%

Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration

Perveen

Vanni

Iacono

et al. 2023

Cells

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“…The excess of cardiac remodeling is also very much affected by the quality of cardiac wound healing and the cellular and molecular profile of the viable myocardium. The comprehensive reviews on advances in the development of immune-modulating therapeutic interventions targeting specific inflammatory pathways following MI, novel strategies to promote therapeutic angiogenesis in the infarcted area, and systemic or localized delivery of anti-fibrotics, including the approaches to inhibit myofibroblast formation that favorably influences wound healing and repair after MI have been published recently [1,[70][71][72][73]. Due to mainly pathophysiological heterogeneity in human patients, however, clinical validation of these novel strategies faces a challenge.…”

Section: Cardiac Molecular Imaging In Therapeutic Applicationsmentioning

confidence: 99%

Nuclear Molecular Imaging of Cardiac Remodeling after Myocardial Infarction

Varasteh

Rischpler

2022

Pharmaceuticals

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The role of molecular imaging technologies in detecting, evaluating, and monitoring cardiovascular disease and their treatment is expanding rapidly. Gradually replacing the conventional anatomical or physiological approaches, molecular imaging strategies using biologically targeted markers provide unique insight into pathobiological processes at molecular and cellular levels and allow for cardiovascular disease evaluation and individualized therapy. This review paper will discuss currently available and developing molecular-based single-photon emission computed tomography (SPECT) and positron emission tomography (PET) imaging strategies to evaluate post-infarction cardiac remodeling. These approaches include potential targeted methods of evaluating critical biological processes, such as inflammation, angiogenesis, and scar formation.

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“…To address this loss of coronary ECs, increasing EC resilience and/or induction of angiogenesis, i.e. sprouting of new blood vessels, have been a target of recent studies with the goal of restoring microcirculation to limit or prevent post-MI cardiac remodeling [ 34 , 60 ]. Reactive oxygen species (ROS) have been shown to be of special pathophysiological importance in EC survival and proliferation in health and disease as well as in CVD including ischemic myocardium [ 20 , 40 , 44 ].…”

Section: Introductionmentioning

confidence: 99%

Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction

et al. 2023

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Recent studies demonstrated that mitochondrial antioxidant MnSOD that reduces mitochondrial (mito) reactive oxygen species (ROS) helps maintain an optimal balance between sub-cellular ROS levels in coronary vascular endothelial cells (ECs). However, it is not known whether EC-specific mito-ROS modulation provides resilience to coronary ECs after a non-reperfused acute myocardial infarction (MI). This study examined whether a reduction in endothelium-specific mito-ROS improves the survival and proliferation of coronary ECs in vivo. We generated a novel conditional binary transgenic animal model that overexpresses (OE) mitochondrial antioxidant MnSOD in an EC-specific manner (MnSOD-OE). EC-specific MnSOD-OE was validated in heart sections and mouse heart ECs (MHECs). Mitosox and mito-roGFP assays demonstrated that MnSOD-OE resulted in a 50% reduction in mito-ROS in MHEC. Control and MnSOD-OE mice were subject to non-reperfusion MI surgery, echocardiography, and heart harvest. In post-MI hearts, MnSOD-OE promoted EC proliferation (by 2.4 ± 0.9 fold) and coronary angiogenesis (by 3.4 ± 0.9 fold), reduced myocardial infarct size (by 27%), and improved left ventricle ejection fraction (by 16%) and fractional shortening (by 20%). Interestingly, proteomic and Western blot analyses demonstrated upregulation in mitochondrial complex I and oxidative phosphorylation (OXPHOS) proteins in MnSOD-OE MHECs. These MHECs also showed increased mitochondrial oxygen consumption rate (OCR) and membrane potential. These findings suggest that mito-ROS reduction in EC improves coronary angiogenesis and cardiac function in non-reperfused MI, which are associated with increased activation of OXPHOS in EC-mitochondria. Activation of an energy-efficient mechanism in EC may be a novel mechanism to confer resilience to coronary EC during MI. Supplementary Information The online version contains supplementary material available at 10.1007/s00395-022-00976-x.

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Targeting angiogenesis in myocardial infarction: Novel therapeutics (Review)

Cited by 24 publications

References 116 publications

Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration

Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration

Nuclear Molecular Imaging of Cardiac Remodeling after Myocardial Infarction

Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction

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