NanotizedPPARαOverexpression Targeted to Hypertrophied Myocardium Improves Cardiac Function by Attenuating the p53-GSK3β-Mediated Mitochondrial Death Pathway | Zendy

Santanu Rana | Zendy; Ritwik Datta | Zendy; Ratul Datta Chaudhuri | Zendy; Emeli Chatterjee | Zendy; Mamta ChawlaSarkar | Zendy; Sagartirtha Sarkar | Zendy

Open Access

NanotizedPPARαOverexpression Targeted to Hypertrophied Myocardium Improves Cardiac Function by Attenuating the p53-GSK3β-Mediated Mitochondrial Death Pathway

Author(s) -

Santanu Rana,

Ritwik Datta,

Ratul Datta Chaudhuri,

Emeli Chatterjee,

Mamta ChawlaSarkar,

Sagartirtha Sarkar

Publication year - 2018

Publication title -

antioxidants and redox signaling

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.277

H-Index - 190

eISSN - 1557-7716

pISSN - 1523-0864

DOI - 10.1089/ars.2017.7371

Subject(s) - downregulation and upregulation , medicine , peroxisome proliferator activated receptor , endocrinology , myocyte , biology , oxidative stress , gsk 3 , muscle hypertrophy , mitochondrion , apoptosis , microbiology and biotechnology , receptor , signal transduction , biochemistry , gene

Metabolic remodeling of cardiac muscles during pathological hypertrophy is characterized by downregulation of fatty acid oxidation (FAO) regulator, peroxisome proliferator-activated receptor alpha (PPARα). Thereby, we hypothesized that a cardiac-specific induction of PPARα might restore the FAO-related protein expression and resultant energy deficit. In the present study, consequences of PPARα augmentation were evaluated for amelioration of chronic oxidative stress, myocyte apoptosis, and cardiac function during pathological cardiac hypertrophy.

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