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Rafiq Research

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Rafiq Research

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Publications
Team

Contact

Name: Khadija Rafiq, PhD

Position: Assistant Professor of Medicine, Division of Cardiology

Organization: Department of Medicine

1020 Locust Street
JAH, Room 543A
Philadelphia, PA 19107

Email: Khadija.Rafiq@jefferson.edu

Contact Number(s):

215-503-5593

Highlighted Publications

Shukla SK, Liu W, Sikder K, Addya S, Sarkar A, Wei Y, Rafiq K. HMGCS2 is a key ketogenic enzyme potentially involved in type 1 diabetes with high cardiovascular risk. Scientific Reports. 2017:4;7(1):4590. PMCID: PMC5496911

Shukla SK, Sikder K, Sarkar A, Addya S, Rafiq K. Molecular network, pathway, and functional analysis of time-dependent gene changes related to cathepsin G exposure in neonatal rat cardiomyocytes. Gene. 2018: S0378-1119(18)30621-8. PMCID: PMC6269229

Sikder K, Shukla SK, Patel N, Singh H, Rafiq K. High Fat Diet Upregulates Fatty Acid Oxidation and Ketogenesis via Intervention of PPAR-γ. Cell Physiol Biochem. 2018;48(3):1317-1331. PMCID: PMC6179152

Amrita Sarkar, Sanket K. Shukla, Anil Kumar,Sankar Addya, Alexander Y. Tsygankov, Khadija Rafiq. The role of allograft inflammatory factor-1 in the effects of experimental diabetes on B cell functions in the heart. Front Cardiovasc Med. 2018 Sep 11;5:126. PMCID: PMC6145033

Kolpakov MA, Sikder K, Sarkar A, Chaki S, Shukla SK, Guo X, Qi Z, Barbery C, Sabri A, Rafiq K. Inflammatory Serine Proteases Play a Critical Role in the Early Pathogenesis of Diabetic Cardiomyopathy. Cell Physiol Biochem. 2019;53(6):982-998. PMCID: PMC6956403

Recent Publications

Sepsis-induced cardiac dysfunction: Gender bias role of allograft inflammatory factor-1

Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction

Proteasome biology and therapeutics in cardiac diseases

Humoral immunity in heart failure

Nanoparticle based treatment for cardiovascular diseases

The Role of Allograft Inflammatory Factor-1 in the Effects of Experimental Diabetes on B Cell Functions in the Heart

Molecular network, pathway, and functional analysis of time-dependent gene changes related to cathepsin G exposure in neonatal rat cardiomyocytes

High Fat Diet Upregulates Fatty Acid Oxidation and Ketogenesis via Intervention of PPAR-γ

Improvement in Therapeutic Efficacy and Reduction in Cellular Toxicity: Introduction of a Novel Anti-PSMA-Conjugated Hybrid Antiandrogen Nanoparticle

HMGCS2 is a key ketogenic enzyme potentially involved in type 1 diabetes with high cardiovascular risk

Dual inhibition of cathepsin G and chymase reduces myocyte death and improves cardiac remodeling after myocardial ischemia reperfusion injury

Protease-activated receptor 4 deficiency offers cardioprotection after acute ischemia reperfusion injury

C-Cbl inhibition improves cardiac function and survival in response to myocardial ischemia

Beta1-adrenergic receptors promote focal adhesion signaling downregulation and myocyte apoptosis in acute volume overload

c-Cbl ubiquitin ligase regulates focal adhesion protein turnover and myofibril degeneration induced by neutrophil protease cathepsin G

Pleiotropic effects of neutrophils on myocyte apoptosis and left ventricular remodeling during early volume overload

Left ventricular remodeling with exercise in hypertension

Novel mode for neutrophil protease cathepsin G-mediated signaling: Membrane shedding of epidermal growth factor is required for cardiomyocyte anoikis

Sympathetic activation causes focal adhesion signaling alteration in early compensated volume overload attributable to isolated mitral regurgitation in the dog

Role of protein-tyrosine phosphatase SHP2 in focal adhesion kinase down-regulation during neutrophil cathepsin G-induced cardiomyocytes anoikis

Immune complex-mediated antigen presentation induces tumor immunity

Regulation of the IL-10 production by human T cells

Effects of co-stimulation by CD58 on human T cell cytokine production: A selective cytokine pattern with induction of high IL-10 production

Differences in regulatory pathways identify subgroups of T cell-derived Th2 cytokines

Naive human T cells can be a source of IL-4 during primary immune responses

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