MétaCan
Menu
Back to cohort
Record W943861060 · doi:10.11575/prism/27108

NLRP3 in Renal Injury and Inflammation

2014· dissertation· en· W943861060 on OpenAlexfundno aff
Akosua Vilaysane

Bibliographic record

VenuePRISM (University of Calgary) · 2014
Typedissertation
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicInflammasome and immune disorders
Canadian institutionsnot available
FundersCanadian Institutes of Health ResearchCanadian Society of NephrologyAmerican Society of Nephrology
KeywordsRenal injuryInflammationMedicineInternal medicineKidney

Abstract

fetched live from OpenAlex

Renal cell injury, death and inflammation are hallmarks of chronic kidney disease (CKD). Unresolved inflammation can chronically damage renal tissue resulting in fibrosis and kidney failure. The Nlrp3 inflammasome has been implicated in the innate immune response to cellular injury and represents a potentially important pathway in the pathogenesis of CKD. The central hypothesis of this thesis is that NLRP3 plays a significant role in renal inflammation and chronic renal injury. In a mouse model of progressive renal injury and fibrosis (unilateral ureteral obstruction, UUO), Nlrp3 expression and inflammasome activation were increased in injured kidneys. Compared to wild-type counterparts, Nlrp3-/-mice undergoing UUO displayed reduced renal injury, fibrosis and inflammatory cytokine levels confirming an important role for Nlrp3 in experimental kidney disease. Bone marrow chimeras in the UUO model indicated that in addition to its inflammasome-forming capabilities in leukocytes, Nlrp3 may play a novel role in the renal epithelial compartment. Indeed, Nlrp3 expression was found in both human and mouse primary tubular epithelial cells. Unlike the inflammasome-forming capability of Nlrp3 in macrophages, renal tubular epithelial cells lacked the components of the inflammasome including caspase-1 and its substrate IL-1β. Rather, Nlrp3 primarily regulated caspase-8 activation and apoptosis in these cells. Experiments to elucidate the mechanism of Nlrp3- regulated caspase-8 activation and apoptosis suggested the involvement of Asc, but not inflammatory cytokines, caspase-1 or caspase-11. Furthermore, Nlrp3-/- tubular epithelial cells were found to have impaired mitochondrial ROS production that was linked to decreased caspase-8 activation during apoptosis. Taken together, results from this thesis identify a significant and multidimensional role for Nlrp3 in the pathogenesis of kidney disease. First, Nlrp3 inflammasome activation in macrophages releases cytokines such as IL-1β and IL-18 that cause renal inflammation, fibrosis and tubular epithelial cell apoptosis. Second, Nlrp3 expressed in tubular epithelial cells displays an intrinsic inflammasome-independent function to regulate caspase-8, mitochondrial ROS and apoptosis. These data identify Nlrp3 as an important player in renal injury and potential therapeutic target for CKD.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: none
Teacher disagreement score0.002
Threshold uncertainty score0.007

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0010.001
Science and technology studies0.0000.001
Scholarly communication0.0010.001
Open science0.0000.001
Research integrity0.0010.002
Insufficient payload (model declined to judge)0.0020.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.003
GPT teacher head0.187
Teacher spread0.184 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2014
Admission routes1
Has abstractyes

Explore more

Same venuePRISM (University of Calgary)Same topicInflammasome and immune disordersFrench-language works237,207