Doroudgar Lab publications

In chronological order

mTORC1 inhibition impairs activation of the unfolded protein response and induces cell death during ER stress in cardiomyocytes
The mechanistic target of rapamycin complex 1 (mTORC1) is a central regulator of protein synthesis that senses and responds to a …
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VARS2 depletion leads to activation of the integrated stress response and disruptions in mitochondrial fatty acid oxidation
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IRE1/XBP1 and Endoplasmic Reticulum Signaling--From Basic to Translational Research for Cardiovascular Disease
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Identification of dynamic RNA-binding proteins uncovers a Cpeb4-controlled regulatory cascade during pathological cell growth of cardiomyocytes
RNA-binding proteins (RBPs) control critical aspects of cardiomyocyte function, but the repertoire of active RBPs in cardiomyocytes …
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Muscle-specific Cand2 is translationally upregulated by mTORC1 and promotes adverse cardiac remodeling
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A multi-network comparative analysis of transcriptome and translatome identifies novel hub genes in cardiac remodeling
Our understanding of the transition from physiological to pathological cardiac hypertrophy remains elusive and largely based on …
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ER stress-induced secretion of proteins and their extracellular functions in the heart
Endoplasmic reticulum (ER) stress is a result of conditions that imbalance protein homeostasis or proteostasis at the ER, for example …
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Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response
The effects of ER stress on protein secretion by cardiac myocytes are not well understood. In this study, the ER stressor thapsigargin …
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Mesencephalic astrocyte-derived neurotrophic factor is an ER-resident chaperone that protects against reductive stress in the heart
We have previously demonstrated that ischemia/reperfusion (I/R) impairs endoplasmic reticulum (ER)-based protein folding in the heart …
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Saraf-dependent activation of mTORC1 regulates cardiac growth
Pathological cardiac hypertrophy is an independent risk for heart failure (HF) and sudden death. Deciphering signaling pathways …
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CRISPR-mediated activation of endogenous gene expression in the postnatal heart
RATIONALE: Genome editing by CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 is evolving rapidly. Recently, …
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TIP30 counteracts cardiac hypertrophy and failure by inhibiting translational elongation
Pathological cardiac overload induces myocardial protein synthesis and hypertrophy, which predisposes to heart failure. To inhibit …
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Monitoring cell-type-specific gene expression using ribosome profiling in vivo during cardiac hemodynamic stress
RATIONALE: Gene expression profiles have been mainly determined by analysis of transcript abundance. However, these analyses cannot …
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Protein misfolding in cardiac disease
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ATF6 regulates cardiac hypertrophy by transcriptional induction of the mTORC1 activator, rheb
RATIONALE: Endoplasmic reticulum (ER) stress dysregulates ER proteostasis, which activates the transcription factor, ATF6 (activating …
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Cardiovascular adverse events in multiple myeloma patients
Multiple myeloma is a malignant disease, caused by an uncontrolled clonal proliferation of a specific group of white blood cells, the …
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S100A4 as a target of the E3-ligase Asb2β and its effect on engineered heart tissue
Background: S100A4 has recently emerged as an important player in cardiac disease, affecting phenotype development in animal models of …
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ATF6 decreases myocardial ischemia/reperfusion damage and links ER stress and oxidative stress signaling pathways in the heart
RATIONALE: Endoplasmic reticulum (ER) stress causes the accumulation of misfolded proteins in the ER, activating the transcription …
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Junctophilin-2 gene therapy rescues heart failure by normalizing RyR2-mediated Ca2+ release
BACKGROUND: Junctophilin-2 (JPH2) is the primary structural protein for the coupling of transverse (T)-tubule associated cardiac L-type …
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S100A4 protects the myocardium against ischemic stress
BACKGROUND: Myocardial infarction is followed by cardiac dysfunction, cellular death, and ventricular remodeling, including tissue …
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Hrd1 and ER-associated protein degradation, ERAD, are critical elements of the adaptive ER stress response in cardiac myocytes
RATIONALE: Hydroxymethyl glutaryl-coenzyme A reductase degradation protein 1 (Hrd1) is an endoplasmic reticulum (ER)-transmembrane E3 …
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PRAS40 prevents development of diabetic cardiomyopathy and improves hepatic insulin sensitivity in obesity
Diabetes is a multi-organ disease and diabetic cardiomyopathy can result in heart failure, which is a leading cause of morbidity and …
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Mechanistic target of rapamycin complex 2 protects the heart from ischemic damage
BACKGROUND: The mechanistic target of rapamycin (mTOR) comprises 2 structurally distinct multiprotein complexes, mTOR complexes 1 and 2 …
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Pathological hypertrophy amelioration by PRAS40-mediated inhibition of mTORC1
Mechanistic target of rapamycin complex 1 (mTORC1), necessary for cellular growth, is regulated by intracellular signaling mediating …
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Regulation of cardiac hypertrophic signaling by prolyl isomerase Pin1
RATIONALE: Cardiac hypertrophy results from the complex interplay of differentially regulated cascades based on the phosphorylation …
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New concepts of endoplasmic reticulum function in the heart: programmed to conserve
Secreted and membrane proteins play critical roles in myocardial health and disease. Studies in non-myocytes have shown that the …
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ATF6 [corrected] and thrombospondin 4: the dynamic duo of the adaptive endoplasmic reticulum stress response
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Limitation of individual folding resources in the ER leads to outcomes distinct from the unfolded protein response
ER stress leads to upregulation of multiple folding and quality control components, known as the unfolded protein response (UPR). …
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Mesencephalic astrocyte-derived neurotrophic factor protects the heart from ischemic damage and is selectively secreted upon sarco/endoplasmic reticulum calcium depletion
The endoplasmic reticulum (ER) stress protein mesencephalic astrocyte-derived neurotrophic factor (MANF) has been reported to protect …
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The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart
Intercellular communication depends on many factors, including proteins released via the classical or non-classical secretory pathways, …
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Ischemia activates the ATF6 branch of the endoplasmic reticulum stress response
Stresses that perturb the folding of nascent endoplasmic reticulum (ER) proteins activate the ER stress response. Upon ER stress, …
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