Yiqiang Cai, PhD, MD
Associate Research Scientist (Nephrology)DownloadHi-Res Photo
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Nephrology
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Associate Research Scientist (Nephrology)
Biography
Dr. Cai graduated from Hunan Medical University in China (M.D. equivalent) and Tokushima University School of Medicine in Japan (Ph.D.). His primary research interest is on the study of polycystic kidney disease with current focus on the molecular basis of the PKD pathogenesis. Dr. Cai is the co-author of more than 40 publications that published in well known professional journals including "Science", "Nature Genetics" (4 papers), "Cell", "Nature Cell Biology", "Science Signaling", "Journal of Clinical Investigation", "Journal of Biological Chemistry", "PNAS" (In press), and others which have been cited by more than 6500 articles (google scholar/2023). Dr. Cai is the recipient of the American Heart Association Scientist Development Award (grant) (2001-2004), the PKD Foundation Research Grant (2005-2006), the Travel Award of the American Society of Nephrology (six times, 2005, 2008, 2009, 2010, 2011, & 2013), and The Jared Grantham Symposium Travel Award (2014). Dr. Cai is the invited reviewer for many professional journals such as the "Journal of American Society of Nephrology", "Kidney International", "Cancer Letter", "Human Molecular Genetics", and others. Dr. Cai is the invited speaker by many Institutions/conference in USA, Japan, Canada, Korea, Netherlands, and in China. Dr. Cai was honored as the "Guest Professor" by the Southern Medical University and the Central South University respectively in China (2008-2012/2013).
Appointments
Nephrology
Associate Research ScientistPrimary
Other Departments & Organizations
- Internal Medicine
- Nephrology
- Somlo Laboratory
Education & Training
- PhD
- Tokushima University School of Medicine (1995)
- MD
- Hunan Medical University (1987)
Research
Overview
My current research is focused on the study of molecular basis of ADPKD pathogenesis. By establishing cell-based model and BAC-transgenic mouse model, we are trying to answer the following questions: 1) How are polycystin-1 and polycystin-2 trafficking to cilia regulated; 2) What is the consequence that trafficking defect of the polycystins cause in the cystogenesis/PKD pathogenesis; 3) What is the molecular basis underlying the mutations of PKD1 and PKD2 genes, 4) How is the polycystin-2 phosphorylation regulated, and 5) What is the role that regulation of polycystin-2 phosphorylation plays on the PKD pathogenesis.
Medical Subject Headings (MeSH)
Congenital, Hereditary, and Neonatal Diseases and Abnormalities; Diseases
ORCID
0000-0001-9632-7275
Research at a Glance
Yale Co-Authors
Frequent collaborators of Yiqiang Cai's published research.
Publications Timeline
A big-picture view of Yiqiang Cai's research output by year.
Stefan Somlo, MD
Sorin Fedeles, PhD, MBA
Ke Dong, MD, MS
Michael Caplan, PhD, MD
Xin Tian, MD
Miguel Coca-Prados, PhD
43Publications
5,880Citations
Publications
2024
Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease
Zhang C, Rehman M, Tian X, Pei S, Gu J, Bell T, Dong K, Tham M, Cai Y, Wei Z, Behrens F, Jetten A, Zhao H, Lek M, Somlo S. Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease. Nature Communications 2024, 15: 3698. PMID: 38693102, PMCID: PMC11063051, DOI: 10.1038/s41467-024-48025-6.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsMouse models of autosomal dominant polycystic kidney diseaseModel of autosomal dominant polycystic kidney diseasePolycystin signalingAutosomal dominant polycystic kidney diseasePolycystin-1Polycystic kidney diseaseTreat autosomal dominant polycystic kidney diseaseGlis2Primary ciliaKidney tubule cellsSignaling pathwayMouse modelDominant polycystic kidney diseasePotential therapeutic targetTranslatomeAntisense oligonucleotidesKidney diseasePolycystinMouse kidneyFunctional effectorsCyst formationTherapeutic targetInactivationFunctional targetPharmacological targetsA synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress
Fedeles B, Bhardwaj R, Ishikawa Y, Khumsubdee S, Krappitz M, Gubina N, Volpe I, Andrade D, Westergerling P, Staudner T, Campolo J, Liu S, Dong K, Cai Y, Rehman M, Gallagher A, Ruchirawat S, Croy R, Essigmann J, Fedeles S, Somlo S. A synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2317344121. PMID: 38241440, PMCID: PMC10823221, DOI: 10.1073/pnas.2317344121.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCyst cellsAutosomal dominant polycystic kidney diseaseMouse models of autosomal dominant polycystic kidney diseasePolycystic kidney diseaseModel of autosomal dominant polycystic kidney diseaseKidney diseaseDeveloped primersMitochondrial oxidative stressPathophysiology of autosomal dominant polycystic kidney diseaseOxidative stressInduce apoptosisMitochondrial respirationCystic cellsUp-regulating aerobic glycolysisHomozygous inactivationMonogenic causeDominant polycystic kidney diseaseAerobic glycolysisRenal replacement therapyApoptosisEnd-stage kidney diseaseAnti-tumor agentsAdult mouse modelChronic kidney diseaseAlkylate DNA
2023
Inactivation of Ire1alpha Endoribonuclease Domain Slows Down ADPKD in Orthologous Mouse Models
Bhardwaj R, Volpe I, Yilmaz D, Pioppini C, Roy K, Rehman M, Cai Y, Krappitz M, Somlo S, Fedeles S. Inactivation of Ire1alpha Endoribonuclease Domain Slows Down ADPKD in Orthologous Mouse Models. Journal Of The American Society Of Nephrology 2023, 34: 19-19. DOI: 10.1681/asn.20233411s119b.Peer-Reviewed Original ResearchDephosphorylation Facilitates Trafficking of Mutant Polycystin-2 to Cilia
Cai Y, Dong K, Spitzer M, Geiges L, Tian X, Krappitz M, Diggs L, Wei Z, Cordido A, Pei S, Fedeles S, Somlo S. Dephosphorylation Facilitates Trafficking of Mutant Polycystin-2 to Cilia. Journal Of The American Society Of Nephrology 2023, 34: 560-560. DOI: 10.1681/asn.20233411s1560b.Peer-Reviewed Original Research
2022
Pkd2 Re-Expression Can Reverse Liver Cysts and Improve GFR in Mouse Models of Autosomal Dominant Polycystic Kidney Disease
Dong K, Tham M, Cordido A, Cai Y, Pei S, Bhardwaj R, Wei Z, Rehman M, Roy K, Tian X, Somlo S. Pkd2 Re-Expression Can Reverse Liver Cysts and Improve GFR in Mouse Models of Autosomal Dominant Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2022, 33: 418-418. DOI: 10.1681/asn.20223311s1418c.Peer-Reviewed Original ResearchXBP1 Activation Reduces Severity of Polycystic Kidney Disease due to a Nontruncating Polycystin-1 Mutation in Mice
Krappitz M, Bhardwaj R, Dong K, Staudner T, Yilmaz DE, Pioppini C, Westergerling P, Ruemmele D, Hollmann T, Nguyen TA, Cai Y, Gallagher AR, Somlo S, Fedeles S. XBP1 Activation Reduces Severity of Polycystic Kidney Disease due to a Nontruncating Polycystin-1 Mutation in Mice. Journal Of The American Society Of Nephrology 2022, 34: 110-121. PMID: 36270750, PMCID: PMC10101557, DOI: 10.1681/asn.2021091180.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsPolycystin-1Polycystin-2Functional polycystin-1Amino acid substitution mutationsAutosomal dominant polycystic kidney diseaseIntegral membrane proteinsTranscription factor XBP1Unfolded protein responsePost-translational maturationAcid substitution mutationsEndoplasmic reticulum chaperoneCiliary traffickingXBP1 activityChaperone functionIntegral membraneActive XBP1Polycystic kidney diseaseMembrane proteinsPC1 functionsPrimary ciliaProtein responseHypomorphic mutationsTransgenic activationSubstitution mutationsTransgenic expression
2021
Interdependent Regulation of Polycystin Expression Influences Starvation-Induced Autophagy and Cell Death
Decuypere JP, Van Giel D, Janssens P, Dong K, Somlo S, Cai Y, Mekahli D, Vennekens R. Interdependent Regulation of Polycystin Expression Influences Starvation-Induced Autophagy and Cell Death. International Journal Of Molecular Sciences 2021, 22: 13511. PMID: 34948309, PMCID: PMC8706473, DOI: 10.3390/ijms222413511.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsProximal tubular epithelial cellsAutosomal dominant polycystic kidney diseaseEarly-stage ADPKD patientsCell deathPC2 expressionDominant polycystic kidney diseaseTubular epithelial cellsRenal cell survivalPolycystin-1Polycystic kidney diseaseCell survivalPolycystin-2Basal autophagyAutophagic cell survivalCell death resistanceADPKD progressionKidney diseaseADPKD patientsLess cell deathPC1 levelsChronic starvationHealthy individualsDuct cellsEpithelial cellsDeath
2019
Polycystin 2 regulates mitochondrial Ca2+ signaling, bioenergetics, and dynamics through mitofusin 2
Kuo IY, Brill AL, Lemos FO, Jiang JY, Falcone JL, Kimmerling EP, Cai Y, Dong K, Kaplan DL, Wallace DP, Hofer AM, Ehrlich BE. Polycystin 2 regulates mitochondrial Ca2+ signaling, bioenergetics, and dynamics through mitofusin 2. Science Signaling 2019, 12 PMID: 31064883, PMCID: PMC6855602, DOI: 10.1126/scisignal.aat7397.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEndoplasmic reticulumPC2 knockdownMitochondrial CaCell culture modelKnockdown of Mfn2Polycystin-2 functionsHuman ADPKD kidneysAutosomal dominant polycystic kidney diseaseKey mitochondrial proteinsAberrant cell proliferationMitochondria-ER contactsCell proliferationER-mitochondrial interfaceKidney cystsIntimate functional relationshipNumerous fluid-filled cystsMitochondrial proteinsCyst-lining epithelial cellsMitofusin 2 expressionCulture modelPolycystin-2Knockdown cellsMitochondrial biogenesisMitofusin 2Mitochondrial respiration
2016
Polycystic Kidney Disease
Cai Y. Polycystic Kidney Disease. 2016, 3653-3658. DOI: 10.1007/978-3-662-46875-3_4667.Peer-Reviewed Original Research
2014
Altered trafficking and stability of polycystins underlie polycystic kidney disease
Cai Y, Fedeles SV, Dong K, Anyatonwu G, Onoe T, Mitobe M, Gao JD, Okuhara D, Tian X, Gallagher AR, Tang Z, Xie X, Lalioti MD, Lee AH, Ehrlich BE, Somlo S. Altered trafficking and stability of polycystins underlie polycystic kidney disease. Journal Of Clinical Investigation 2014, 124: 5129-5144. PMID: 25365220, PMCID: PMC4348948, DOI: 10.1172/jci67273.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsG-protein-coupled receptor proteolytic sitePolycystic kidney diseaseKidney diseaseGPS cleavageAutosomal dominant polycystic kidney diseaseMissense mutationsDominant polycystic kidney diseasePolycystin-1Polycystin-2Murine modelSevere formPathogenic missense mutationsPKD1 mutationsCOOH-terminal fragmentDiseaseMissense variantsExpression levelsFunctional assaysCell-based systemsAltered trafficking
Academic Achievements & Community Involvement
activity linking the defect of ciliary trafficking to a genetic kidney cystic disease: insights on a potential pharmaceutical target for ADPKD
Oral Presentation3rd annual Sapporo Summer Seminar for One Health (SaSSOH), JapanDetails09/16/2015 - PresentSapporo, Hokkaido Prefecture, JapanSponsored by Hokkaido University, JapanAbstract/Synopsisinvited speaker
honor The Jared Grantham Symposium Travel Award
National AwardThe Jared Grantham Symposium planning committeeDetails07/09/2014United Statesactivity Modified BAC-transgene: a powerful tool for studies of gene function and genetic diseases
Oral PresentationThe Sun Yat-sen International Forum on Bio-Medicine, ChinaDetails11/22/2013 - PresentGuangzhou, Guangdong, ChinaSponsored by Sun Yat-sen Medical University, ChinaAbstract/Synopsisinvited speaker
honor Advances in Research Conference Travel Award
National AwardAmerican Society of NephrologyDetails11/05/2013, 11/03/2011, 11/15/2010, 10/27/2009, 11/03/2008, 08/06/2005United Statesactivity The long way toward understanding of polycystic kidney disease
Oral PresentationThe 2013 academic annual meeting of Oncology Group of Chinese Society of Oral and Maxillofacial SurgeryDetails06/22/2013 - 06/23/2013Changsha, Hunan, ChinaSponsored by Central South University, ChinaAbstract/Synopsisinvited speaker
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