Publications by authors named "Reika Langanki"
Article Synopsis
- Phosphodiesterase 3A gain-of-function mutations lead to hypertension and stroke, but surprisingly do not cause cardiac hypertrophy or heart failure in affected patients, suggesting a potential protective mechanism in the heart.* -
- Researchers used CRISPR-Cas9 models and human stem cells to analyze the effects of these mutations, observing that new mutations could enhance enzyme activity and self-assembly while preserving normal heart structure despite high blood pressure.* -
- In their experiments, cardiac responses in mutant models showed adaptive changes in calcium cycling and similarities in heart function to normal (wild-type) rats, indicating the mutations might lead to beneficial heart adaptations under certain conditions.*
Background: High blood pressure is the primary risk factor for cardiovascular death worldwide. Autosomal dominant hypertension with brachydactyly clinically resembles salt-resistant essential hypertension and causes death by stroke before 50 years of age. We recently implicated the gene encoding phosphodiesterase 3A (); however, in vivo modeling of the genetic defect and thus showing an involvement of mutant PDE3A is lacking.
View Article and Find Full Text PDFWe previously identified a quantitative trait locus (QTL) for stroke proneness between the kallikrein (Klk) and Mt1pa markers on rat chromosome 1. To gain functional insights, we constructed congenic strains by introgressing either the whole or selected chromosomal segments from the stroke-prone (SHRsp) onto the stroke-resistant (SHRsr) spontaneously hypertensive rat genome and vice versa. The phenotype was the latency to develop stroke under a Japanese high-salt, low-potassium diet for 3 mo [known as Japanese diet (JD)].
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