Angela Lorts

ORCID: 0000-0003-1447-5456
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About
Contact & Profiles
Research Areas
  • Mechanical Circulatory Support Devices
  • Cardiac Structural Anomalies and Repair
  • Congenital Heart Disease Studies
  • Cardiac Arrest and Resuscitation
  • Transplantation: Methods and Outcomes
  • Heart Failure Treatment and Management
  • Cardiac pacing and defibrillation studies
  • Cardiomyopathy and Myosin Studies
  • Renal Transplantation Outcomes and Treatments
  • Muscle Physiology and Disorders
  • Organ Transplantation Techniques and Outcomes
  • Cardiac Arrhythmias and Treatments
  • Adolescent and Pediatric Healthcare
  • Cardiac Fibrosis and Remodeling
  • Cardiovascular Effects of Exercise
  • Neurogenetic and Muscular Disorders Research
  • Cardiovascular Issues in Pregnancy
  • Pulmonary Hypertension Research and Treatments
  • Childhood Cancer Survivors' Quality of Life
  • Congenital Anomalies and Fetal Surgery
  • Cardiac electrophysiology and arrhythmias
  • Cardiovascular Function and Risk Factors
  • Signaling Pathways in Disease
  • Organ Donation and Transplantation
  • Viral Infections and Immunology Research

Cincinnati Children's Hospital Medical Center
2016-2025

University of Cincinnati
2015-2025

University of Cincinnati Medical Center
2016-2024

International Society for Heart and Lung Transplantation
2024

IFC Research (United Kingdom)
2024

Children's Medical Center
2010-2023

Cincinnati Sportsmedicine and Orthopaedic Center
2021

Boston Children's Hospital
2019

Indiana University – Purdue University Indianapolis
2007-2017

Indiana University School of Medicine
2007-2017

The cardiac extracellular matrix is a dynamic structural support network that both influenced by, and regulator of, pathological remodeling hypertrophic growth. In response to pathologic insults, the adult heart reexpresses secreted protein periostin (Pn). Here we show Pn critically involved in regulating response, interstitial fibrosis, ventricular following long-term pressure overload stimulation myocardial infarction. Mice lacking gene encoding ( Postn ) were more prone rupture first 10...

10.1161/circresaha.107.149047 article EN Circulation Research 2007-06-15

Significance Duchenne muscular dystrophy (DMD) is a rare and devastating muscle disease caused by mutations in the X-linked DMD gene (which encodes dystrophin protein). Serum biomarkers hold significant potential as objective phenotypic measures of state, well pharmacological effects response to therapeutic interventions. Here we describe proteomics approach determine serum levels 1,125 proteins 93 patients 45 controls. The study identified 44 that differed significantly between These data...

10.1073/pnas.1507719112 article EN Proceedings of the National Academy of Sciences 2015-05-26

The muscular dystrophies are broadly classified as muscle wasting diseases with myofiber dropout due to cellular necrosis, inflammation, alterations in extracellular matrix composition, and fatty cell replacement. These events transpire progress despite ongoing regeneration from endogenous satellite cells. degeneration/regeneration response injury/disease is modulated by the proinflammatory cytokine transforming growth factor-β (TGF-β), which can also profoundly influence composition through...

10.1073/pnas.1204708109 article EN Proceedings of the National Academy of Sciences 2012-06-18

Improving the outcomes of pediatric patients with congenital heart disease end-stage failure depends on collaboration all stakeholders; this includes providers, and families, industry representatives. Because rarity condition heterogeneity etiologies that occur at centers, learnings must be shared between institutions disciplines to move field forward. To foster collaboration, excel discovery, bring data bedside, a new, collaborative quality improvement science network—ACTION (Advanced...

10.1097/mat.0000000000001133 article EN ASAIO Journal 2020-02-21

Following a pathological insult, the adult mammalian heart undergoes hypertrophic growth and remodeling of extracellular matrix. Although small subpopulation cardiomyocytes can reenter cell cycle following cardiac injury, myocardium is largely thought to be incapable significant regeneration. Periostin, an matrix protein, has recently been proposed induce reentry differentiated back into promote meaningful repair myocardial infarction. Here, we show that although periostin induced in it does...

10.1161/circresaha.108.188649 article EN Circulation Research 2008-11-27

Thrombotic and bleeding complications have historically been major causes of morbidity mortality in pediatric ventricular assist device (VAD) support. Standard anticoagulation with unfractionated heparin is fraught problems related to its heterogeneous biochemical composition unpredictable pharmacokinetics. We sought describe the utilization outcomes children paracorporeal VAD support who are treated direct thrombin inhibitors (DTIs) antithrombosis therapy. Retrospective multicenter review...

10.1097/mat.0000000000001093 article EN ASAIO Journal 2019-11-20

Periostin is a secreted protein that can alter extracellular matrix remodeling in response to tissue injury. However, the functional role of periostin development atherosclerotic plaques has yet be described despite its observed induction diseased vessels and presence serum.Hyperlipidemic, apolipoprotein E-null mice (ApoE(-/) (-)) were crossed with (Postn(-/-)) gene-deleted placed on high-fat diet for 6 or 14 weeks induce atherosclerosis. En face analysis aortas showed significantly...

10.1161/atvbaha.115.306397 article EN Arteriosclerosis Thrombosis and Vascular Biology 2015-11-13

Background— Left ventricular noncompaction (LVNC) can occur in isolation or co-occur with a cardiomyopathy phenotype cardiovascular malformation. The yield of gene panel testing infants, children, and adolescents diagnosis LVNC is unknown. By characterizing pediatric population LVNC, we sought to determine the testing, distinguish for without co-occurring cardiac findings, define additional factors influencing genetic yield. Methods Results— One hundred twenty-eight individuals diagnosed at...

10.1161/circgenetics.117.001735 article EN Circulation Cardiovascular Genetics 2017-12-01

Abstract Optimising short- and long-term outcomes for children patients with CHD depends on continued scientific discovery translation to clinical improvements in a coordinated effort by multiple stakeholders. Several challenges remain clinicians, researchers, administrators, patients, families seeking continuous advancements the field. We describe new integrated research improvement network – Cardiac Networks United that seeks build upon experience success achieved to-date create...

10.1017/s1047951118001683 article EN Cardiology in the Young 2018-12-20
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