Evidence map›Paper›PMID 42819575›Full record

ArticleAnnual review of cancer biology2020

Mitophagy and Mitochondrial Dysfunction in Cancer.

Kay F Macleod

Abstract read
In one paragraph

Article in Annual review of cancer biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Mechanisms of breast cancer metastasis.Clinical & experimental metastasis · 2022
    Review
  4. Review
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

1 author.

Kay F MacleodThe Ben May Department for Cancer Research, University of Chicago, Chicago, Illinois 60637, USA.

Funding

Functions of BNIP3 in lipid metabolism in the liver and in hepatocellular carcinomaR01CA200310 · NCI · UNIVERSITY OF CHICAGO · PI KAY F MACLEOD · 2016 to 2026
$3.6M
(PQ5) Consequences of imbalanced mitophagy and mitochondrial biogenesis in cancerR01CA216242 · NCI · UNIVERSITY OF CHICAGO · PI MACLEOD, KAY F · 2017 to 2021
$1.6M
Functions of BNIP3 in Mammary TumorigenesisR01CA131188 · NCI · UNIVERSITY OF CHICAGO · PI MACLEOD, KAY F · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA131188NCI NIH HHS R01 CA200310NCI NIH HHS R01 CA216242
6 · The paper itself

Abstract

The process of mitophagy, in which mitochondria are selectively turned over at the autophagolysosome, plays a central role in both eliminating dysfunctional mitochondria and reducing mitochondrial mass as an adaptive response to key physiological stresses, such as hypoxia, nutrient deprivation, and DNA damage. Defects in mitophagy have been linked to altered mitochondrial metabolism, production of excess reactive oxygen species and ferroptosis, heightened inflammasome activation, altered cell fate decisions, and senescence, among other cellular consequences. Consequently, functional mitophagy contributes to proper tissue differentiation and repair and metabolic homeostasis, limiting inflammatory responses and modulating tumor progression and metastasis. This review examines the major pathways that control mitophagy, including PINK1-dependent mitophagy and BNIP3/NIX-dependent mitophagy. It also discusses the cellular signaling mechanisms used to sense mitochondrial dysfunction to activate mitophagy and how defective mitophagy results in deregulated tumor cell growth and cancer.

Indexed as

BNIP3cGAS-STINGDNA damageDRP1electron transport chainferroptosisinflammasomeMiDASmitochondrial depolarizationmitochondrial fissionmitophagyNAD+NIXParkinPINK1reactive oxygen species

Identifiers

PMID42819575
PMCPMC13626216

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.