Evidence map›Paper›PMID 36451821›Full record

ArticleFrontiers in immunology2022

The mitochondrial gene-CMPK2 functions as a rheostat for macrophage homeostasis.

Prabhakar Arumugam, Meghna Chauhan, Thejaswitha Rajeev, Rahul Chakraborty, Kanika Bisht, Mahima Madan, Deepthi Shankaran, Sivaprakash Ramalingam, Sheetal Gandotra, Vivek Rao

Abstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
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  3. p21Nature aging · 2026
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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

10 authors.

Prabhakar ArumugamImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Meghna ChauhanImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Thejaswitha RajeevImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Rahul ChakrabortyImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Kanika BishtImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Mahima MadanImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Deepthi ShankaranImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Sivaprakash RamalingamImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Sheetal GandotraImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.
Vivek RaoImmunology and Infectious Disease Unit, Council of Scientific and Industrial Research (CSIR)- Institute of Genomics and Integrative Biology, New Delhi, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to their role in cellular energy production, mitochondria are increasingly recognized as regulators of the innate immune response of phagocytes. Here, we demonstrate that altering expression levels of the mitochondria-associated enzyme, cytidine monophosphate kinase 2 (CMPK2), disrupts mitochondrial physiology and significantly deregulates the resting immune homeostasis of macrophages. Both CMPK2 silenced and constitutively overexpressing macrophage lines portray mitochondrial stress with marked depolarization of their membrane potential, enhanced reactive oxygen species (ROS), and disturbed architecture culminating in the enhanced expression of the pro-inflammatory genes IL1β, TNFα, and IL8. Interestingly, the long-term modulation of CMPK2 expression resulted in an increased glycolytic flux of macrophages akin to the altered physiological state of activated M1 macrophages. While infection-induced inflammation for restricting pathogens is regulated, our observation of a total dysregulation of basal inflammation by bidirectional alteration of CMPK2 expression only highlights the critical role of this gene in mitochondria-mediated control of inflammation.

Indexed as

Genes, MitochondrialMacrophagesHomeostasisHumansInflammationNucleoside-Phosphate Kinasecytidylate kinaseNucleoside-Phosphate KinaseCMPK2immuno-metabolisminfectionM1 macrophagemitochondria

Identifiers

PMID36451821
PMCPMC9702992

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.