Satadru K. Lahiri

ORCID: 0000-0001-9502-1530
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About
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Research Areas
  • Kruppel-like factors research
  • Cardiac electrophysiology and arrhythmias
  • Atrial Fibrillation Management and Outcomes
  • Ion channel regulation and function
  • Cardiomyopathy and Myosin Studies
  • Cancer-related gene regulation
  • Cardiac Fibrosis and Remodeling
  • Signaling Pathways in Disease
  • MicroRNA in disease regulation
  • Genetic Syndromes and Imprinting
  • Calpain Protease Function and Regulation
  • Viral Infections and Immunology Research
  • Mitochondrial Function and Pathology
  • Cancer-related molecular mechanisms research
  • Cell Adhesion Molecules Research
  • ATP Synthase and ATPases Research
  • Cardiac Ischemia and Reperfusion
  • Chronic Myeloid Leukemia Treatments
  • RNA and protein synthesis mechanisms
  • TGF-β signaling in diseases
  • RNA Research and Splicing
  • CRISPR and Genetic Engineering
  • Cardiac Arrhythmias and Treatments
  • Pulmonary Hypertension Research and Treatments
  • Calcium signaling and nucleotide metabolism

Baylor College of Medicine
2018-2025

Cardiovascular Institute Hospital
2021-2024

University of Minnesota
2024

University of Central Florida
2012-2022

Florida College
2012-2022

Institute of Molecular Biology and Biophysics
2021

Huazhong University of Science and Technology
2021

Tongji Hospital
2021

Chronic kidney disease (CKD) is associated with a higher risk of atrial fibrillation (AF). The mechanistic link between CKD and AF remains elusive. Interleukin (IL)-1β, main effector 'NLR-family pyrin domain-containing 3' (NLRP3) inflammasome activation, key modulator conditions inflammation, such as CKD. Circulating IL-1β levels were elevated in CKD-patients vs sinus rhythm. Moreover, NLRP3-activity was enhanced atria CKD-patients. To elucidate the role NLRP3/IL-1β signaling pathogenesis...

10.1172/jci167517 article EN cc-by Journal of Clinical Investigation 2023-08-15

Rationale: Autosomal-dominant mutations in ryanodine receptor type 2 ( RYR2 ) are responsible for ≈60% of all catecholaminergic polymorphic ventricular tachycardia. Dysfunctional RyR2 subunits trigger inappropriate calcium leak from the tetrameric channel resulting potentially lethal In vivo CRISPR/Cas9-mediated gene editing is a promising strategy that could be used to eliminate disease-causing Ryr2 allele and hence rescue Objective: To determine if somatic genome using CRISPR/Cas9 system...

10.1161/circresaha.118.313369 article EN Circulation Research 2018-09-28

Enhanced diastolic calcium (Ca2+) release through ryanodine receptor type-2 (RyR2) has been implicated in atrial fibrillation (AF) promotion. Diastolic sarcoplasmic reticulum Ca2+ leak is caused by increased RyR2 phosphorylation PKA (protein kinase A) or CaMKII (Ca2+/calmodulin-dependent kinase-II) phosphorylation, less dephosphorylation protein phosphatases. However, considerable controversy remains regarding the molecular mechanisms underlying altered function AF. We thus aimed to...

10.1161/circulationaha.120.045791 article EN Circulation 2020-07-20

Abnormal calcium (Ca2+) release from the sarcoplasmic reticulum (SR) contributes to pathogenesis of atrial fibrillation (AF). Increased phosphorylation 2 proteins essential for normal SR-Ca2+ cycling, type-2 ryanodine receptor (RyR2) and phospholamban (PLN), enhances susceptibility AF, but underlying mechanisms remain unclear. Protein phosphatase 1 (PP1) limits steady-state both RyR2 PLN. Proteomic analysis uncovered a novel PP1-regulatory subunit (PPP1R3A [PP1 regulatory type 3A]) in...

10.1161/circulationaha.119.039642 article EN Circulation 2019-06-12

Side effects of radiation therapy (RT) remain the most challenging issue for pancreatic cancer treatment. Cerium oxide nanoparticles (CONPs) are currently being tested in pre-clinical trials as an adjuvant to sensitize cells RT and protect normal tissues from harmful side effects. CONPs were not able significantly affect RT-induced DNA damage cells, thereby ruling out sensitization through increased mitotic catastrophe. However, activation c-Jun terminal kinase (JNK), a key driver apoptosis,...

10.3390/cancers10090303 article EN Cancers 2018-09-01

Myocardial lipid metabolism is critical to normal heart function, whereas altered regulation has been linked cardiac diseases including cardiomyopathies. Genetic variants in the JPH2 gene can cause hypertrophic cardiomyopathy (HCM) and, some cases, dilated (DCM). In this study, we tested hypothesis that identified patients with HCM and DCM, respectively, distinct alterations myocardial profiles. Echocardiography revealed clinically significant dysfunction both knock-in mouse models of...

10.26508/lsa.202302330 article EN cc-by Life Science Alliance 2024-03-04

BACKGROUND: In heart failure, signaling downstream the β2-adrenergic receptor is critical. Sympathetic stimulation of alters cAMP (cyclic adenosine 3′,5′-monophosphate) and triggers PKA (protein kinase A)-dependent phosphorylation proteins that regulate cardiac function. levels are regulated in part by PDEs (phosphodiesterases). Several AKAPs (A anchoring proteins) function proposed as targets for precise pharmacology. AKAP12 expressed has been reported to directly bind receptor, PKA, PDE4D....

10.1161/circresaha.123.323655 article EN Circulation Research 2024-03-20

Krüppel-like factor 8 (KLF8) regulates critical gene transcription and cellular events associated with cancer. However, the role of KLF8 in cancer remains largely unknown. Here, we report a surprisingly novel for DNA repair breast cells. Comet, clonogenic, WST-1 assays showed that expression is required protecting human cells from doxorubicin-induced damage cell death. Western blotting indicated overexpression ectopic attenuated levels marker γH2A.X doxorubicin-treated PARP-1(+/+) but not...

10.1074/jbc.m112.418053 article EN cc-by Journal of Biological Chemistry 2012-10-29

// Tianshu Li 1, 2 , Heng Lu 1 Debarati Mukherjee Satadru K. Lahiri Chao Shen 3 Lin Yu Jihe Zhao Burnett School of Biomedical Sciences, University Central Florida College Medicine, Orlando, FL, USA Department Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, Life Wuhan University, Wuhan, China Correspondence to: Zhao, e-mail: Jihe.Zhao@ucf.edu Keywords: KLF8, EGFR, microRNA141, invasion and metastasis, breast cancer Received: March 17, 2015 Accepted: May 14,...

10.18632/oncotarget.4077 article EN Oncotarget 2015-05-27

// Debarati Mukherjee 1, * , Heng Lu Lin Yu 1 Chunjiang He 2 Satadru K. Lahiri Tianshu Li 3 Jihe Zhao Burnett School of Biomedical Sciences, University Central Florida College Medicine, Orlando, FL, USA Basic Medical Wuhan University, Wuhan, China Current address: Cleveland Clinic, Cleveland, OH, These authors contributed equally to this work Correspondence to: Zhao, e-mail: Jihe.Zhao@ucf.edu Keywords: KLF8, CXCR4, transendothelial migration, invasion, metastasis Received: November 07,...

10.18632/oncotarget.8083 article EN Oncotarget 2016-03-14

Abstract Aims Abnormal intracellular calcium (Ca2+) handling contributes to the progressive nature of atrial fibrillation (AF), most common sustained cardiac arrhythmia. Evidence in mouse models suggests that activation nuclear factor activated T-cell (NFAT) signalling pathway remodelling. Our aim was determine role NFATc2 AF humans and models. Methods results Expression levels NFATc1–c4 isoforms were assessed by quantitative reverse transcription–polymerase chain reaction right appendages...

10.1093/cvr/cvab325 article EN Cardiovascular Research 2021-10-12

Introduction: Heterozygous autosomal-dominant single nucleotide variants in RYR2 account for 60% of cases catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited arrhythmia disorder associated with high mortality rates. CRISPR/Cas9-mediated genome editing is a promising therapeutic approach that can permanently cure the disease by removing mutant allele. However, safety and long-term efficacy this strategy have not been established relevant model. Aim: The purpose study...

10.20517/jca.2023.42 article EN The Journal of Cardiovascular Aging 2024-01-05

Heart failure (HF) is a complex disease with rising prevalence despite advances in treatment. Protein phosphatase 1 (PP1) has long been implicated HF pathogenesis, but its exact role both unclear and controversial. Most previous studies measured only the PP1 catalytic subunit (PP1c) without investigating diverse set of interactors, which confer localization substrate specificity to holoenzyme. In this study, we define interactome cardiac tissue test hypothesis that becomes rearranged during...

10.1161/circulationaha.118.034361 article EN Circulation 2018-04-18
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