Wound healing, fibroblast heterogeneity, and fibrosis.

Cardiac fibrosis: Myofibroblast-mediated pathological regulation and drug delivery strategies

Mechanical communication in fibrosis progression

The adult mammalian heart contains abundant interstitial and perivascular fibroblasts that expand following injury and play a reparative role but also contribute to maladaptive fibrotic remodeling. Following myocardial infarction, cardiac fibroblasts undergo dynamic phenotypic transitions, contributing to the regulation of inflammatory, reparative, and angiogenic responses. This review manuscript discusses the mechanisms of regulation, roles and fate of fibroblasts in the infarcted heart. During the inflammatory phase of infarct healing, the release of alarmins by necrotic cells promotes a pro-inflammatory and matrix-degrading fibroblast phenotype that may contribute to leukocyte recruitment. The clearance of dead cells and matrix debris from the infarct stimulates anti-inflammatory pathways and activates transforming growth factor (TGF)-β cascades, resulting in the conversion of fibroblasts to α-smooth muscle actin (α-SMA)-expressing myofibroblasts. Activated myofibroblasts secrete large amounts of matrix proteins and form a collagen-based scar that protects the infarcted ventricle from catastrophic complications, such as cardiac rupture. Moreover, infarct fibroblasts may also contribute to cardiac repair by stimulating angiogenesis. During scar maturation, fibroblasts disassemble α-SMA+ stress fibers and convert to specialized cells that may serve in scar maintenance. The prolonged activation of fibroblasts and myofibroblasts in the infarct border zone and in the remote remodeling myocardium may contribute to adverse remodeling and to the pathogenesis of heart failure. In addition to their phenotypic plasticity, fibroblasts exhibit remarkable heterogeneity. Subsets with distinct phenotypic profiles may be responsible for the wide range of functions of fibroblast populations in infarcted and remodeling hearts.

/pdf/properties-and-functions-of-fibroblasts-and-myofibroblasts-2dtl4oay.pdf

Properties and Functions of Fibroblasts and Myofibroblasts in Myocardial Infarction

Fibroblast and myofibroblast activation in normal tissue repair and fibrosis.

Background: Cardiac fibroblasts (CFs) have a central role in the ventricular remodeling process associated with different types of fibrosis. Recent studies have shown that fibroblasts do not respon...

https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.119.044557

Single-Cell RNA Sequencing Analysis Reveals a Crucial Role for CTHRC1 (Collagen Triple Helix Repeat Containing 1) Cardiac Fibroblasts After Myocardial Infarction.

Ablación endoepicárdica de taquicardia ventricular con un nuevo navegador no fluoroscópico de alta densidad

Ablation of ventricular tachycardia (VT) is a procedure that is becoming increasingly more widespread in clinical practice. It is estimated that 12% to 17% of cases of VT are of myocardial and subepicardial origin, which is a more common substrate in nonischemic heart disease. Rhythmia (Boston Scientific; Marlborough, Massachusetts, United States) is a new nonfluoroscopic navigation system able to generate high-density maps combining a steerable 64-electrode catheter (IntellaMap Orion; Boston Scientific) with software able to automatically capture the recorded electrograms. Given the novelty of the system, experience with this catheter for epicardial mapping is very limited, and no information has been published on the outcomes and complications of VT ablation guided by the Rhythmia system. We present the case of a 56-year-old physician who was an endurance sports enthusiast. He started to experience frequent episodes of palpitations, generally triggered by exercise, and accompanied by nausea. On exercise testing, regular sustained broad QRS tachycardia was induced with right bundle branch block and left superior axis morphology. In the 24-hour Holter recording, 80 episodes of the same tachycardia were detected. The results of both echocardiography and coronary angiography were normal, and diagnosis of VT was confirmed in an electrophysiology study. On magnetic resonance imaging, a 30 7-mm area of gadolinium enhancement was observed between the myocardium and subepicardium of the inferior wall of the left ventricle.

Endoepicardial Ventricular Tachycardia Ablation With a New High-density Non-fluoroscopic Navigation System.

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Single-Cell RNA Sequencing Analysis Reveals a Crucial Role for CTHRC1 (Collagen Triple Helix Repeat Containing 1) Cardiac Fibroblasts After Myocardial Infarction.

Ablación endoepicárdica de taquicardia ventricular con un nuevo navegador no fluoroscópico de alta densidad

Endoepicardial Ventricular Tachycardia Ablation With a New High-density Non-fluoroscopic Navigation System.