FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2169165514> ?p ?o ?g. }

• W2169165514 endingPage "R141" @default.
• W2169165514 startingPage "R131" @default.
• W2169165514 abstract "Cystic fibrosis (CF) is a recessive genetic disease caused by mutations in the CF transmembrane conductance regulator ( CFTR ). CFTR is primarily present in epithelial cells of the airways, intestine and in cells with exocrine and endocrine functions. Mutations in the gene encoding the channel protein complex (CFTR) cause alterations in the ionic composition of secretions from the lung, gastrointestinal tract, liver, and also the pancreas. CF-related diabetes (CFRD), the most common complication of CF, has a major detrimental impact on pulmonary function, nutrition and survival. Glucose derangements in CF seem to start from early infancy and, even when the pathophysiology is multifactorial, insulin insufficiency is clearly a major component. Consistently, recent evidence has confirmed that CFTR is an important regulator of insulin secretion by islet β-cells. In addition, several other mechanisms were also recognized from cellular and animals models also contributing to either β-cell mass reduction or β-cell malfunction. Understanding such mechanisms is crucial for the development of the so-called ‘transformational’ therapies in CF, including the preservation of insulin secretion. Innovative therapeutic approaches aim to modify specific CFTR mutant proteins or positively modulate their function. CFTR modulators have recently shown in vitro capacity to enhance insulin secretion and thereby potential clinical utility in CFDR, including synergistic effects between corrector and potentiator drugs. The introduction of incretins and the optimization of exocrine pancreatic replacement complete the number of therapeutic options of CFRD besides early diagnosis and implementation of insulin therapy. This review focuses on the recently identified pathogenic mechanisms leading to CFRD relevant for the development of novel pharmacological avenues in CFRD therapy." @default.
• W2169165514 created "2016-06-24" @default.
• W2169165514 creator A5017315671 @default.
• W2169165514 date "2015-04-01" @default.
• W2169165514 modified "2023-09-24" @default.
• W2169165514 title "MANAGEMENT OF ENDOCRINE DISEASE: Cystic fibrosis-related diabetes: novel pathogenic insights opening new therapeutic avenues" @default.
• W2169165514 cites W1504967583 @default.
• W2169165514 cites W1559981541 @default.
• W2169165514 cites W1965179792 @default.
• W2169165514 cites W1965463808 @default.
• W2169165514 cites W1965576398 @default.
• W2169165514 cites W1969881162 @default.
• W2169165514 cites W1972007591 @default.
• W2169165514 cites W1978110685 @default.
• W2169165514 cites W1980164139 @default.
• W2169165514 cites W1985619693 @default.
• W2169165514 cites W1990670389 @default.
• W2169165514 cites W1991078379 @default.
• W2169165514 cites W1992500371 @default.
• W2169165514 cites W1992729193 @default.
• W2169165514 cites W1995390066 @default.
• W2169165514 cites W1998496055 @default.
• W2169165514 cites W2001314764 @default.
• W2169165514 cites W2004438949 @default.
• W2169165514 cites W2008985050 @default.
• W2169165514 cites W2014843857 @default.
• W2169165514 cites W2015044617 @default.
• W2169165514 cites W2018982025 @default.
• W2169165514 cites W2019338701 @default.
• W2169165514 cites W2021193933 @default.
• W2169165514 cites W2024967740 @default.
• W2169165514 cites W2027823440 @default.
• W2169165514 cites W2032407253 @default.
• W2169165514 cites W2035131077 @default.
• W2169165514 cites W2036820990 @default.
• W2169165514 cites W2039599894 @default.
• W2169165514 cites W2041993512 @default.
• W2169165514 cites W2042399870 @default.
• W2169165514 cites W2045994112 @default.
• W2169165514 cites W2051330706 @default.
• W2169165514 cites W2059300085 @default.
• W2169165514 cites W2059516713 @default.
• W2169165514 cites W2062552675 @default.
• W2169165514 cites W2063363172 @default.
• W2169165514 cites W2067891202 @default.
• W2169165514 cites W2077619599 @default.
• W2169165514 cites W2079929562 @default.
• W2169165514 cites W2080318972 @default.
• W2169165514 cites W2082293476 @default.
• W2169165514 cites W2088600987 @default.
• W2169165514 cites W2099252894 @default.
• W2169165514 cites W2101073077 @default.
• W2169165514 cites W2102496493 @default.
• W2169165514 cites W2103879666 @default.
• W2169165514 cites W2104754533 @default.
• W2169165514 cites W2111187716 @default.
• W2169165514 cites W2114854928 @default.
• W2169165514 cites W2115046089 @default.
• W2169165514 cites W2115461616 @default.
• W2169165514 cites W2116707205 @default.
• W2169165514 cites W2120043611 @default.
• W2169165514 cites W2120361612 @default.
• W2169165514 cites W2125240189 @default.
• W2169165514 cites W2126108368 @default.
• W2169165514 cites W2132547736 @default.
• W2169165514 cites W2133708874 @default.
• W2169165514 cites W2135446403 @default.
• W2169165514 cites W2140868856 @default.
• W2169165514 cites W2142006298 @default.
• W2169165514 cites W2145394445 @default.
• W2169165514 cites W2146114441 @default.
• W2169165514 cites W2147821592 @default.
• W2169165514 cites W2150297577 @default.
• W2169165514 cites W2162033607 @default.
• W2169165514 cites W2162275257 @default.
• W2169165514 cites W2162836078 @default.
• W2169165514 cites W2165705148 @default.
• W2169165514 cites W2893460811 @default.
• W2169165514 doi "https://doi.org/10.1530/eje-14-0644" @default.
• W2169165514 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25336504" @default.
• W2169165514 hasPublicationYear "2015" @default.
• W2169165514 type Work @default.
• W2169165514 sameAs 2169165514 @default.
• W2169165514 citedByCount "35" @default.
• W2169165514 countsByYear W21691655142015 @default.
• W2169165514 countsByYear W21691655142016 @default.
• W2169165514 countsByYear W21691655142017 @default.
• W2169165514 countsByYear W21691655142018 @default.
• W2169165514 countsByYear W21691655142019 @default.
• W2169165514 countsByYear W21691655142020 @default.
• W2169165514 countsByYear W21691655142021 @default.
• W2169165514 countsByYear W21691655142022 @default.
• W2169165514 crossrefType "journal-article" @default.
• W2169165514 hasAuthorship W2169165514A5017315671 @default.
• W2169165514 hasBestOaLocation W21691655141 @default.
• W2169165514 hasConcept C103395026 @default.
• W2169165514 hasConcept C126322002 @default.
• W2169165514 hasConcept C134018914 @default.

• next