Evidence map›Paper›PMID 34970493›Full record

ArticleFrontiers in oncology2021

Mitochondrial Ndufa4l2 Enhances Deposition of Lipids and Expression of Ca9 in the TRACK Model of Early Clear Cell Renal Cell Carcinoma.

Kristian B Laursen, Qiuying Chen, Francesca Khani, Nabeel Attarwala, Steve S Gross, Lukas Dow, David M Nanus, Lorraine J Gudas

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 36% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Kristian B LaursenDepartment of Pharmacology, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
Qiuying ChenDepartment of Pharmacology, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
Francesca KhaniDepartment of Pathology and Laboratory Medicine, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
Nabeel AttarwalaDepartment of Pharmacology, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
Steve S GrossDepartment of Pharmacology, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
Lukas DowDepartment of Medicine, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
David M NanusDepartment of Urology, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
Lorraine J GudasDepartment of Pharmacology, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States.
Cornell University · USPresbyterian Hospital · USNew York Hospital Queens · USWeill Cornell Medicine · US

Funding

Gene Nutrient Interactions in Kidney FunctionR01DK113088 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUDAS, LORRAINE J · 2018 to 2025
$3.7M
NIDDK NIH HHS R01 DK113088
6 · The paper itself

Abstract

Mitochondrial dysfunction and aberrant glycolysis are hallmarks of human clear cell renal cell carcinoma (ccRCC). Whereas glycolysis is thoroughly studied, little is known about the mitochondrial contribution to the pathology of ccRCC. Mitochondrial Ndufa4l2 is predictive of poor survival of ccRCC patients, and in kidney cancer cell lines the protein supports proliferation and colony formation. Its role in ccRCC, however, remains enigmatic. We utilized our established ccRCC model, termed Transgenic Cancer of the Kidney (TRACK), to generate a novel genetically engineered mouse model in which dox-regulated expression of an shRNA decreases Ndufa4l2 levels specifically in the renal proximal tubules (PT). This targeted knockdown of Ndufa4l2 reduced the accumulation of neutral renal lipid and was associated with decreased levels of the ccRCC markers carbonic anhydrase 9 (CA9) and Enolase 1 (ENO1). These findings suggest a link between mitochondrial dysregulation (i.e. high levels of Ndufa4l2), lipid accumulation, and the expression of ccRCC markers ENO1 and CA9, and demonstrate that lipid accumulation and ccRCC development can potentially be attenuated by inhibiting Ndufa4l2.

Indexed as

clear cell renal cell carcinomaHIF1hypoxialipidsmitochondriaproximal tubulesvon Hippel-Lindau

Identifiers

PMID34970493
PMCPMC8712948
OpenAlexW4200052297

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.