Publications by authors named "J J Nigro"

Repair or palliation of pulmonary atresia with intact ventricular septum (PA/IVS) often falls into one of 4 categories: cardiac transplant, 2-ventricular circulation, 1.5 ventricle circulation, or single ventricle circulation. The optimal management strategy has been an area of much debate.

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Background: Double outlet right ventricle (DORV) is a challenging congenital cardiac lesion to surgically master. We utilize computed tomography-guided-three-dimensional (3D) modeling/printing and novel in-house software to delineate anatomical relationships providing operative insight into the surgical approach. Our intent is to highlight this and showcase our technology.

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Article Synopsis
  • Protein quality control (PQC) is essential for the function of heart cells, and certain mutations (like R120G in CRYAB and P209L in BAG3) can lead to the buildup of harmful protein aggregates and heart diseases.
  • The study explored how these protein aggregates are taken up by mitochondria and removed through a process called mitophagy, especially in mice lacking the TRAF2 protein, which is necessary for mitophagy.
  • Results showed that without TRAF2, there was an increase in protein aggregates and misplacement of other proteins, indicating that proper mitophagy is critical for preventing cardiac dysfunction.
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Myocardial infarction initiates cardiac remodeling and is central to heart failure pathogenesis. Following myocardial ischemia-reperfusion injury, monocytes enter the heart and differentiate into diverse subpopulations of macrophages. Here we show that deletion of Hif1α, a hypoxia response transcription factor, in resident cardiac macrophages led to increased remodeling and overrepresentation of macrophages expressing arginase 1 (Arg1).

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Mesenchymal stromal cells (MSC) are promising stem cell therapy for treating cardiovascular and other degenerative diseases. Diabetes affects the functional capability of MSC and impedes cell-based therapy. Despite numerous studies, the impact of diabetes on MSC myocardial reparative activity, metabolic fingerprint, and the mechanism of dysfunction remains inadequately perceived.

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