AGTR2 absence or antagonism prevents cystic fibrosis pulmonary manifestations

Journal of Cystic Fibrosis

Volumn 18, Issue 1, 2019, Pages 127-134

  Darrah, Rebecca J ^a,b   Jacono, Frank J ^b,c   Joshi, Neha ^b   Mitchell, Anna L ^b   Sattar, Abdus ^b   Campanaro, Cara K ^b   Litman, Paul ^a   Frey, Jennifer ^b   Nethery, David E ^c   Barbato, Eric S ^a   Hodges, Craig A ^b   Corvol, Harriet ^d,e   Cutting, Garry R ^f   Knowles, Michael R ^g   Strug, Lisa J ^h,i   Drumm, Mitchell L ^b  

^a CASE WESTERN RESERVE UNIVERSITY   (United States)

^b CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c LOUIS STOKES CLEVELAND VA MEDICAL CENTER   (United States)

^d SORBONNE UNIVERSITÉ   (France)

^e ARMAND TROUSSEAU HOSPITAL   (France)

^f JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^g UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

^h HOSPITAL FOR SICK CHILDREN   (Canada)

ⁱ UNIVERSITY OF TORONTO   (Canada)

Author keywords

Angiotensin signaling; GWAS follow up; Mouse models of airway disease; Pulmonary function

Indexed keywords

1 (4 DIMETHYLAMINO 3 METHYLBENZYL) 5 DIPHENYLACETYL 4,5,6,7 TETRAHYDRO 1H IMIDAZO[4,5 C]PYRIDINE 6 CARBOXYLIC ACID; ANGIOTENSIN 2 RECEPTOR; ANGIOTENSIN 2 RECEPTOR ANTAGONIST; DNA; IMIDAZOLE DERIVATIVE; PYRIDINE DERIVATIVE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CHILD; CONTROLLED STUDY; CYSTIC FIBROSIS; DRUG ANTAGONISM; FEMALE; FORCED EXPIRATORY FLOW; FORCED EXPIRATORY VOLUME; FORCED VITAL CAPACITY; GENE DELETION; GENE LOCUS; GENETIC ANALYSIS; GENETIC ASSOCIATION; GENOME-WIDE ASSOCIATION STUDY; HUMAN; LUNG DISEASE; LUNG FUNCTION; MAJOR CLINICAL STUDY; MALE; MOUSE; NONHUMAN; PATHOGENESIS; SCHOOL CHILD; SIGNAL TRANSDUCTION; TREATMENT DURATION; X CHROMOSOME; ANIMAL; COMPLICATION; DISEASE MODEL; DNA MUTATIONAL ANALYSIS; DRUG EFFECT; FOLLOW UP; GENETICS; GENOTYPE; KNOCKOUT MOUSE; LUNG; METABOLISM; MUTATION; PATHOPHYSIOLOGY; PHYSIOLOGY; RETROSPECTIVE STUDY;

ANGIOTENSIN II TYPE 2 RECEPTOR BLOCKERS; ANIMALS; CHILD; CYSTIC FIBROSIS; DISEASE MODELS, ANIMAL; DNA; DNA MUTATIONAL ANALYSIS; FEMALE; FOLLOW-UP STUDIES; FORCED EXPIRATORY FLOW RATES; GENOTYPE; HUMANS; IMIDAZOLES; LUNG; LUNG DISEASES; MALE; MICE; MICE, KNOCKOUT; MUTATION; PYRIDINES; RECEPTOR, ANGIOTENSIN, TYPE 2; RETROSPECTIVE STUDIES;

EID: 85048788128     PISSN: 15691993     EISSN: 18735010     Source Type: Journal    
DOI: 10.1016/j.jcf.2018.05.013     Document Type: Article

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