J. Rafael-Fortney

发表

Muscle damage, metabolism, and oxidative stress in mdx mice: Impact of aerobic running

S. Devor, K. E. Schill, Alex R Altenberger, 2016, Muscle & nerve.

Mineralocorticoid Receptor Signaling Contributes to Normal Muscle Repair After Acute Injury

C. Gomez-Sanchez, E. Gomez-Sanchez, Jeovanna Lowe, 2019, Front. Physiol..

Improvement of cardiac contractile function by peptide-based inhibition of NF-κB in the utrophin/dystrophin-deficient murine model of muscular dystrophy

D. Guttridge, J. Rafael-Fortney, Dawn A. Delfín, 2011, Journal of Translational Medicine.

Peptide-Based Inhibition of NF-κB Rescues Diaphragm Muscle Contractile Dysfunction in a Murine Model of Duchenne Muscular Dystrophy

Michael A. Freitas, J. Mendell, P. Robbins, 2011, Molecular medicine.

Utrophin deficiency worsens cardiac contractile dysfunction present in dystrophin-deficient mdx mice.

J. Rafael-Fortney, P. Janssen, Jill A. Rafael-Fortney, 2005, American journal of physiology. Heart and circulatory physiology.

Contemporary Cardiac Issues in Duchenne Muscular Dystrophy

E. Hoffman, D. Judge, G. Pearson, 2015, Circulation.

Lengthening-contractions in isolated myocardium impact force development and worsen cardiac contractile function in the mdx mouse model of muscular dystrophy.

J. Rafael-Fortney, Dawn A. Delfín, P. Janssen, 2011, Journal of applied physiology.

Prednisolone Attenuates Improvement of Cardiac and Skeletal Contractile Function and Histopathology by Lisinopril and Spironolactone in the mdx Mouse Model of Duchenne Muscular Dystrophy

S. Raman, T. Tran, K. E. Schill, 2014, PloS one.

Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model

J. Chamberlain, Jeovanna Lowe, J. Rafael-Fortney, 2021, JCI insight.

Sustaining cardiac claudin-5 levels prevents functional hallmarks of cardiomyopathy in a muscular dystrophy mouse model.

K. E. Schill, J. Rafael-Fortney, Dawn A. Delfín, 2012, Molecular therapy : the journal of the American Society of Gene Therapy.

Mineralocorticoid receptor antagonists improve membrane integrity independent of muscle force in muscular dystrophy.

N. Weisleder, Jeovanna Lowe, J. Rafael-Fortney, 2019, Human molecular genetics.

Advances in Cardiovascular Imaging Cardiac Involvement in Patients With Muscular Dystrophies Magnetic Resonance Imaging Phenotype and Genotypic Considerations

S. Raman, D. Verhaert, J. Rafael-Fortney, 2011 .

Mineralocorticoid receptor antagonism by finerenone is sufficient to improve function in preclinical muscular dystrophy

S. Raman, Jeovanna Lowe, J. Rafael-Fortney, 2020, ESC heart failure.

Is Upregulation of Sarcolipin Beneficial or Detrimental to Muscle Function?

S. Harper, Subash C. Gupta, J. Gunn, 2021, Frontiers in Physiology.

Muscle Twitch Kinetics Are Dependent on Muscle Group, Disease State, and Age in Duchenne Muscular Dystrophy Mouse Models

Jonathan P. Davis, Jeovanna Lowe, J. Rafael-Fortney, 2020, Frontiers in Physiology.

Early Inflammation in Muscular Dystrophy Differs Between Limb and Respiratory Muscles and Increases with Dystrophic Severity.

Jeovanna Lowe, J. Rafael-Fortney, S. Bansal, 2021, The American journal of pathology.

Claudin-5 levels are reduced from multiple cell types in human failing hearts and are associated with mislocalization of ephrin-B1.

V. Fedorov, P. Mohler, A. Kilic, 2015, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

Rationally engineered Troponin C modulates in vivo cardiac function and performance in health and disease

Jonathan P. Davis, Bo Zhang, V. Fedorov, 2016, Nature Communications.

Mineralocorticoid Receptor Signaling in the Inflammatory Skeletal Muscle Microenvironments of Muscular Dystrophy and Acute Injury

J. Rafael-Fortney, Z. Howard, Jill A. Rafael-Fortney, 2022, Frontiers in Pharmacology.

Restoration of all dystrophin protein interactions by functional domains in trans does not rescue dystrophy

K. L. Gardner, J. Rafael-Fortney, J. Edwards, 2006, Gene Therapy.

Haploinsufficiency of utrophin gene worsens skeletal muscle inflammation and fibrosis in mdx mice

R. Ransohoff, Xinyu Zhao, Liping Liu, 2008, Journal of the Neurological Sciences.

Cardiomyopathy in the dystrophin/utrophin-deficient mouse model of severe muscular dystrophy is characterized by dysregulation of matrix metalloproteinases

S. Raman, J. Rafael-Fortney, Dawn A. Delfín, 2012, Neuromuscular Disorders.

Duchenne Muscular Dystrophy Mice and Men: Can Understanding a Genetic Cardiomyopathy Inform Treatment of Other Myocardial Diseases?

S. Raman, J. Rafael-Fortney, Jill A. Rafael-Fortney, 2016, Circulation research.

Somatic gene therapy to treat heart failure is one step closer to reality.

M. Periasamy, J. Rafael-Fortney, 2009, Cardiovascular research.

Mineralocorticoid receptor antagonists and glucocorticoids differentially affect skeletal muscle inflammation and pathology in muscular dystrophy

Jeovanna Lowe, J. Rafael-Fortney, S. Bansal, 2022, JCI insight.

The Angiotensin Converting Enzyme Inhibitor Lisinopril Improves Muscle Histopathology but not Contractile Function in a Mouse Model of Duchenne Muscular Dystrophy

S. Raman, T. Tran, Jeovanna Lowe, 2015, Journal of neuromuscular diseases.

Dystrophin glycoprotein complex dysfunction: a regulatory link between muscular dystrophy and cancer cachexia.

Swarnali Acharyya, M. Hollingsworth, M. Saji, 2005, Cancer cell.

S. Raman, C. Gomez-Sanchez, E. Gomez-Sanchez, 2016, Journal of neuromuscular diseases.

Interplay of IKK/NF-kappaB signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophy.

K. L. Gardner, Swarnali Acharyya, M. Karin, 2007, The Journal of clinical investigation.

Mineralocorticoid Receptor Antagonists in Muscular Dystrophy Mice During Aging and Exercise.

C. Gomez-Sanchez, E. Gomez-Sanchez, Jeovanna Lowe, 2018, Journal of neuromuscular diseases.

Standard Operating Procedures (SOPs) for Evaluating the Heart in Preclinical Studies of Duchenne Muscular Dystrophy

D. Kass, K. Kinnett, D. Duan, 2016, Journal of Cardiovascular Translational Research.

Metabolic Dysfunction and Altered Mitochondrial Dynamics in the Utrophin-Dystrophin Deficient Mouse Model of Duchenne Muscular Dystrophy

Jeovanna Lowe, M. Periasamy, J. Rafael-Fortney, 2015, PloS one.

Gene expression effects of glucocorticoid and mineralocorticoid receptor agonists and antagonists on normal human skeletal muscle.

C. Gomez-Sanchez, E. Gomez-Sanchez, J. Rafael-Fortney, 2017, Physiological genomics.

Mineralocorticoid receptors are present in skeletal muscle and represent a potential therapeutic target

D. Guttridge, C. Gomez-Sanchez, E. Gomez-Sanchez, 2015, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Renin-angiotensin-aldosterone system inhibitors improve membrane stability and change gene-expression profiles in dystrophic skeletal muscles.

S. Bhattacharya, N. Weisleder, Jeovanna Lowe, 2017, American journal of physiology. Cell physiology.

Eplerenone for early cardiomyopathy in Duchenne muscular dystrophy: a randomised, double-blind, placebo-controlled trial

S. Raman, J. Kissel, L. Cripe, 2015, The Lancet Neurology.

Early treatment with lisinopril and spironolactone preserves cardiac and skeletal muscle in Duchenne muscular dystrophy mice.

S. Raman, T. Tran, J. Rafael-Fortney, 2011, Circulation.

Cytoplasmic gamma-actin contributes to a compensatory remodeling response in dystrophin-deficient muscle.

J. Ervasti, J. Rafael-Fortney, Laurin M Hanft, 2006, Proceedings of the National Academy of Sciences of the United States of America.

The force-temperature relationship in healthy and dystrophic mouse diaphragm; implications for translational study design

J. Rafael-Fortney, N. Rastogi, P. Janssen, 2012, Front. Physio..

Myocardial Contractile Dysfunction Is Present without Histopathology in a Mouse Model of Limb-Girdle Muscular Dystrophy-2F and Is Prevented after Claudin-5 Virotherapy

J. Rafael-Fortney, P. Janssen, Jill A. Rafael-Fortney, 2016, Front. Physiol..

Analysis of gene expression differences between utrophin/dystrophin-deficient vs mdx skeletal muscles reveals a specific upregulation of slow muscle genes in limb muscles

J. D. Porter, B. Gong, J. Rafael-Fortney, 2006, Neurogenetics.

CASK and Dlg form a PDZ protein complex at the mammalian neuromuscular junction

J. Rafael-Fortney, Jill A. Rafael-Fortney, Tessily A Mays, 2004, Muscle & nerve.

Truncated CASK does not alter skeletal muscle or protein interactors

J. Rafael-Fortney, P. Janssen, J. Wilson, 2008, Muscle & nerve.

Claudin-5 localizes to the lateral membranes of cardiomyocytes and is altered in utrophin/dystrophin-deficient cardiomyopathic mice.

B. Gong, J. Rafael-Fortney, A. Merriam, 2005, Journal of molecular and cellular cardiology.

Myeloid cells are capable of synthesizing aldosterone to exacerbate damage in muscular dystrophy.

C. Gomez-Sanchez, Steven S. Welc, E. Gomez-Sanchez, 2016, Human molecular genetics.

Claudin-5 levels are reduced in human end-stage cardiomyopathy.

Amit A. Doshi, P. Binkley, K. Margulies, 2008, Journal of molecular and cellular cardiology.

Glutamate receptors localize postsynaptically at neuromuscular junctions in mice

A. Chishti, T. Hanada, J. Rafael-Fortney, 2009, Muscle & nerve.

The lack of Troponin I Ser-23/24 phosphorylation is detrimental to in vivo cardiac function and exacerbates cardiac disease.

N. Weisleder, Jeovanna Lowe, J. Rafael-Fortney, 2023, Journal of molecular and cellular cardiology.

Impairment of Diastolic Function by Lack of Frequency-Dependent Myofilament Desensitizationin Rabbit Right Ventricular Hypertrophy

R. Hamlin, Subash C. Gupta, M. Periasamy, 2009, Circulation. Heart failure.

Micro-dystrophin gene therapy demonstrates long-term cardiac efficacy in a severe Duchenne muscular dystrophy model

J. Chamberlain, Jeovanna Lowe, J. Rafael-Fortney, 2023, Molecular therapy. Methods & clinical development.

CASK localizes to nuclei in developing skeletal muscle and motor neuron culture models and is agrin‐independent

K. L. Gardner, J. Rafael-Fortney, Tessily A Mays, 2006, Journal of cellular physiology.