Shan S. Parikh, MD, PhD
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Clinical Fellow
Biography
Shan Parikh is a clinical fellow in cardiovascular medicine and a member of the Physician-Scientist Research Pathway at Yale School of Medicine. He completed both a medical degree and a Ph.D. from Vanderbilt University. As a Ph.D. student at Vanderbilt (Department of Pharmacology, Vanderbilt Center for Arrhythmia Research and Therapeutics), Shan utilized human induced pluripotent stem cell derived cardiomyocytes for the investigation of contractile dysfunction and arrhythmogenesis in inherited cardiomyopathies. As a physician-scientist at Yale, Shan is interested in investigating cardiac disease and delivering state of the art care to patients with cardiovascular disease.
Last Updated on March 09, 2023.
Departments & Organizations
Education & Training
- Resident
- Yale University (2022)
- MD
- Vanderbilt University School of Medicine (2020)
- PhD
- Vanderbilt University, Pharmacology (2018)
- MS
- University of Connecticut, Physiology and Neurobiology (2011)
- BS
- University of Connecticut , Physiology and Neurobiology (2010)
Board Certifications
Internal Medicine
- Certification Organization
- AB of Internal Medicine
- Original Certification Date
- 2023
Research
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Overview
Medical Research Interests
Cardiovascular Abnormalities; Cardiovascular Diseases; Fatty Liver; Glucose Metabolism Disorders; Heart Diseases; Heart Failure; Vascular Diseases
Public Health Interests
Cardiovascular Diseases; Aging; Metabolism; Obesity
ORCID
0000-0003-1806-9199
Research at a Glance
Publications Timeline
A big-picture view of Shan S. Parikh's research output by year.
19Publications
1,013Citations
Publications
Featured Publications
Impaired Dynamic Sarcoplasmic Reticulum Ca Buffering in Autosomal Dominant CPVT2
Wleklinski M, Kryshtal D, Kim K, Parikh S, Blackwell D, Marty I, Iyer V, Knollmann B. Impaired Dynamic Sarcoplasmic Reticulum Ca Buffering in Autosomal Dominant CPVT2. Circulation Research 2022, 131: 673-686. PMID: 36102198, PMCID: PMC9529867, DOI: 10.1161/circresaha.121.320661.Peer-Reviewed Original ResearchCitationsAltmetricPatient-independent human induced pluripotent stem cell model: A new tool for rapid determination of genetic variant pathogenicity in long QT syndrome
Chavali NV, Kryshtal DO, Parikh SS, Wang L, Glazer AM, Blackwell DJ, Kroncke BM, Shoemaker MB, Knollmann BC. Patient-independent human induced pluripotent stem cell model: A new tool for rapid determination of genetic variant pathogenicity in long QT syndrome. Heart Rhythm 2019, 16: 1686-1695. PMID: 31004778, PMCID: PMC6935564, DOI: 10.1016/j.hrthm.2019.04.031.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLong QT syndromeExtracellular field potentialsQT syndromeHiPSC-CMGenetic testingPluripotent stem cell modelsHiPSC modelsSudden cardiac deathStem cell modelUnrelated healthy volunteersVentricular action potentialPatch-clamp studiesNovel missense variantVoltage-dependent inactivationCardiac deathClinical benefitCommercial genetic testingGenetic variant pathogenicityHealthy volunteersCell modelElectrophysiological propertiesAction potentialsBeating rateUnknown significancePatch clampThyroid and Glucocorticoid Hormones Promote Functional T-Tubule Development in Human-Induced Pluripotent Stem Cell–Derived Cardiomyocytes
Parikh SS, Blackwell DJ, Gomez-Hurtado N, Frisk M, Wang L, Kim K, Dahl CP, Fiane A, Tønnessen T, Kryshtal DO, Louch WE, Knollmann BC. Thyroid and Glucocorticoid Hormones Promote Functional T-Tubule Development in Human-Induced Pluripotent Stem Cell–Derived Cardiomyocytes. Circulation Research 2017, 121: 1323-1330. PMID: 28974554, PMCID: PMC5722667, DOI: 10.1161/circresaha.117.311920.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHuman-induced pluripotent stem cell-derived cardiomyocytesExcitation-contraction couplingPluripotent stem cell-derived cardiomyocytesCa releaseGlucocorticoid hormonesStem cell-derived cardiomyocytesCell-derived cardiomyocytesCa-induced Ca releaseT-tubule developmentAdult human ventricular cardiomyocytesExtensive T-tubule networkHuman ventricular cardiomyocytesL-type Ca channelsL-type CaT-tubulesIntracellular Ca releaseCell-based therapiesConfocal line scanHeart diseaseT-tubule networkFunctional maturationVentricular cardiomyocytesPermissive roleDay 16Ca channels
2023
Regulation of Postnatal Cardiomyocyte Maturation by an RNA Splicing Regulator RBFox1
Huang J, Lee J, Rau C, Pezhouman A, Yokota T, Miwa H, Feldman M, Kong T, Yang Z, Tay W, Pushkarsky I, Kim K, Parikh S, Udani S, Soh B, Gao C, Stiles L, Shirihai O, Knollmann B, Ardehali R, Di Carlo D, Wang Y. Regulation of Postnatal Cardiomyocyte Maturation by an RNA Splicing Regulator RBFox1. Circulation 2023, 148: 1263-1266. PMID: 37844148, PMCID: PMC10593507, DOI: 10.1161/circulationaha.122.061602.Peer-Reviewed Original ResearchCitationsAltmetric
2022
Transcriptional Dysregulation Underlies Both Monogenic Arrhythmia Syndrome and Common Modifiers of Cardiac Repolarization
Bersell K, Yang T, Mosley J, Glazer A, Hale A, Kryshtal D, Kim K, Steimle J, Brown J, Salem J, Campbell C, Hong C, Wells Q, Johnson A, Short L, Blair M, Behr E, Petropoulou E, Jamshidi Y, Benson M, Keyes M, Ngo D, Vasan R, Yang Q, Gerszten R, Shaffer C, Parikh S, Sheng Q, Kannankeril P, Moskowitz I, York J, Wang T, Knollmann B, Roden D. Transcriptional Dysregulation Underlies Both Monogenic Arrhythmia Syndrome and Common Modifiers of Cardiac Repolarization. Circulation 2022, 147: 824-840. PMID: 36524479, PMCID: PMC9992308, DOI: 10.1161/circulationaha.122.062193.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsPlatelet-derived growth factorInduced pluripotent stem cellsBrugada syndromeArrhythmia syndromesSerum platelet-derived growth factorSodium currentGeneral transcriptional mechanismFramingham Heart Study cohortPI3KPDGF receptor expressionLate sodium currentCardiac sodium currentCardiac transcription factorsSmall molecule perturbationsCurrent-clamp experimentsCardiac sodium channel geneSodium channel geneFramingham Heart StudyMurine model systemPluripotent stem cellsMonogenic arrhythmia syndromesReceptor blockadeElectrophysiologic abnormalitiesQTc intervalStudy cohortAutosomal dominant CPVT2 is caused by impaired dynamic calcium buffering in the sarcoplasmic reticulum
Wleklinski M, Parikh S, Kryshtal D, Knollmann B. Autosomal dominant CPVT2 is caused by impaired dynamic calcium buffering in the sarcoplasmic reticulum. Biophysical Journal 2022, 121: 12a-13a. DOI: 10.1016/j.bpj.2021.11.2644.Peer-Reviewed Original Research
2021
Autosomal-Dominant CASQ2-K180R Causes CPVT by Altering Intra-SR Calcium Buffering without Reducing Casq2 Protein Levels
Wleklinski M, Parikh S, Blackwell D, Knollmann B. Autosomal-Dominant CASQ2-K180R Causes CPVT by Altering Intra-SR Calcium Buffering without Reducing Casq2 Protein Levels. Biophysical Journal 2021, 120: 238a-239a. DOI: 10.1016/j.bpj.2020.11.1572.Peer-Reviewed Original ResearchCitations
2020
Autosomal-dominant CASQ2-K180R Causes CPVT by a Different Mechanism than Autosomal-recessive Casq2 Mutations
Wleklinski M, Parikh S, Knollmann B. Autosomal-dominant CASQ2-K180R Causes CPVT by a Different Mechanism than Autosomal-recessive Casq2 Mutations. Biophysical Journal 2020, 118: 101a. DOI: 10.1016/j.bpj.2019.11.709.Peer-Reviewed Original ResearchCitations
2019
An Autosomal Dominant Mutation in Calsequestrin 2 Causes CPVT Without Changing Protein Levels
Wleklinski M, Parikh S, Knollmann B. An Autosomal Dominant Mutation in Calsequestrin 2 Causes CPVT Without Changing Protein Levels. Biophysical Journal 2019, 116: 95a-96a. DOI: 10.1016/j.bpj.2018.11.556.Peer-Reviewed Original ResearchCitationsEstablishing Pathogenicity of Novel LQTS8 Variant via Genomic Editing of Human iPSC
Kryshtal D, Chavali N, Parikh S, Wang L, Glazer A, Shoemaker M, Knollmann B. Establishing Pathogenicity of Novel LQTS8 Variant via Genomic Editing of Human iPSC. Biophysical Journal 2019, 116: 99a. DOI: 10.1016/j.bpj.2018.11.573.Peer-Reviewed Original Research
Clinical Trials
Current Trials
DAL-302
IRB ID2000039690RoleSub InvestigatorPrimary Completion Date08/31/2027Recruiting ParticipantsGenderBothAge45+ years
Academic Achievements & Community Involvement
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Activities
activity TLC-1180 Reverses Obesity, Improves Myocardial Insulin Sensitivity, and Enhances Cardiac Fitness in a Murine Model of Diet-Induced Obesity
01/29/2026 - PresentOral PresentationCardiometabolism in Health and Disease, Keystone SymposiumDetailsKeystone, CO, United States
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