Leukocyte-Dependent Regulation of Cardiac Fibrosis

Okyere, Ama Dedo; Tilley, Douglas G.

doi:10.3389/fphys.2020.00301

Cited by 34 publications

(47 citation statements)

References 143 publications

(256 reference statements)

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“…Thermal ablation induces coagulative necrosis, 14 triggering an inflammatory response with leucocytes. 15 , 16 Once the inflammatory reaction is resolved, activated leucocytes facilitate collagen synthesis by promoting fibroblast activation. 17 Thus, necrosis causes fibrosis through an inflammatory reaction.…”

Section: Discussionmentioning

confidence: 99%

Pulsed field ablation prevents chronic atrial fibrotic changes and restrictive mechanics after catheter ablation for atrial fibrillation

et al. 2021

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Aims Pulsed field ablation (PFA), a non-thermal ablative modality, may show different effects on the myocardial tissue compared to thermal ablation. Thus, this study aimed to compare the left atrial (LA) structural and mechanical characteristics after PFA vs. thermal ablation. Methods and results Cardiac magnetic resonance was performed pre-ablation, acutely (<3 h), and 3 months post-ablation in 41 patients with paroxysmal atrial fibrillation (AF) undergoing pulmonary vein (PV) isolation with PFA (n = 18) or thermal ablation (n = 23, 16 radiofrequency ablations, 7 cryoablations). Late gadolinium enhancement (LGE), T2-weighted, and cine images were analysed. In the acute stage, LGE volume was 60% larger after PFA vs. thermal ablation (P < 0.001), and oedema on T2 imaging was 20% smaller (P = 0.002). Tissue changes were more homogeneous after PFA than after thermal ablation, with no sign of microvascular damage or intramural haemorrhage. In the chronic stage, the majority of acute LGE had disappeared after PFA, whereas most LGE persisted after thermal ablation. The maximum strain on PV antra, the LA expansion index, and LA active emptying fraction declined acutely after both PFA and thermal ablation but recovered at the chronic stage only with PFA. Conclusion Pulsed field ablation induces large acute LGE without microvascular damage or intramural haemorrhage. Most LGE lesions disappear in the chronic stage, suggesting a specific reparative process involving less chronic fibrosis. This process may contribute to a preserved tissue compliance and LA reservoir and booster pump functions.

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Section: Discussionmentioning

confidence: 99%

Pulsed field ablation prevents chronic atrial fibrotic changes and restrictive mechanics after catheter ablation for atrial fibrillation

et al. 2021

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“…Several cells, such as immune cells (macrophages, monocytes, mast cells and lymphocytes), cardiomyocytes and vascular cells, secrete fibrogenic mediators. Among them there are chemokines, cytokines, TGF-β, TNF-α, PDGF, Endothelin (ET)-1, FGF, ROS, the renin-angiotensin-aldosterone system (RAAS) and specific proteases that regulate the fibrotic process ( Frieler and Mortensen, 2015 ; Strassheim et al, 2019 ; Psarras et al, 2019 ; Okyere and Tilley, 2020 ).…”

Section: Organ Fibrosis Emt and Possible Anti-emt Therapeutic Stratementioning

confidence: 99%

The Epithelial-to-Mesenchymal Transition as a Possible Therapeutic Target in Fibrotic Disorders

Gregorio

Robuffo

Spalletta³

et al. 2020

Front. Cell Dev. Biol.

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Fibrosis is a chronic and progressive disorder characterized by excessive deposition of extracellular matrix, which leads to scarring and loss of function of the affected organ or tissue. Indeed, the fibrotic process affects a variety of organs and tissues, with specific molecular background. However, two common hallmarks are shared: the crucial role of the transforming growth factor-beta (TGF-β) and the involvement of the inflammation process, that is essential for initiating the fibrotic degeneration. TGF-β in particular but also other cytokines regulate the most common molecular mechanism at the basis of fibrosis, the Epithelial-to-Mesenchymal Transition (EMT). EMT has been extensively studied, but not yet fully explored as a possible therapeutic target for fibrosis. A deeper understanding of the crosstalk between fibrosis and EMT may represent an opportunity for the development of a broadly effective anti-fibrotic therapy. Here we report the evidences of the relationship between EMT and multi-organ fibrosis, and the possible therapeutic approaches that may be developed by exploiting this relationship.

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“…Qualitative and quantitative modifications of the cardiac microenvironment following cardiac injury result from the crosstalk between a variety of cell types representing the “normal compartment” of the heart, such as fibroblasts, endothelial cells, inflammatory and immune cells, as well as soluble factors and the components of the ECM [ 25 , 26 , 27 ].…”

Section: Introductionmentioning

confidence: 99%

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

Baci

Bosi

Parisi

et al. 2020

IJMS

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Despite relevant advances made in therapies for cardiovascular diseases (CVDs), they still represent the first cause of death worldwide. Cardiac fibrosis and excessive extracellular matrix (ECM) remodeling are common end-organ features in diseased hearts, leading to tissue stiffness, impaired myocardial functional, and progression to heart failure. Although fibrosis has been largely recognized to accompany and complicate various CVDs, events and mechanisms driving and governing fibrosis are still not entirely elucidated, and clinical interventions targeting cardiac fibrosis are not yet available. Immune cell types, both from innate and adaptive immunity, are involved not just in the classical response to pathogens, but they take an active part in “sterile” inflammation, in response to ischemia and other forms of injury. In this context, different cell types infiltrate the injured heart and release distinct pro-inflammatory cytokines that initiate the fibrotic response by triggering myofibroblast activation. The complex interplay between immune cells, fibroblasts, and other non-immune/host-derived cells is now considered as the major driving force of cardiac fibrosis. Here, we review and discuss the contribution of inflammatory cells of innate immunity, including neutrophils, macrophages, natural killer cells, eosinophils and mast cells, in modulating the myocardial microenvironment, by orchestrating the fibrogenic process in response to tissue injury. A better understanding of the time frame, sequences of events during immune cells infiltration, and their action in the injured inflammatory heart environment, may provide a rationale to design new and more efficacious therapeutic interventions to reduce cardiac fibrosis.

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Leukocyte-Dependent Regulation of Cardiac Fibrosis

Cited by 34 publications

References 143 publications

Pulsed field ablation prevents chronic atrial fibrotic changes and restrictive mechanics after catheter ablation for atrial fibrillation

Pulsed field ablation prevents chronic atrial fibrotic changes and restrictive mechanics after catheter ablation for atrial fibrillation

The Epithelial-to-Mesenchymal Transition as a Possible Therapeutic Target in Fibrotic Disorders

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

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