Evidence map›Paper›PMID 35831624›Full record

ReviewCell death and differentiation2022

Targeting mitochondrial metabolism for precision medicine in cancer.

Lourdes Sainero-Alcolado, Judit Liaño-Pons, María Victoria Ruiz-Pérez, Marie Arsenian-Henriksson

Open access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 2 pooled it
27.0field-weighted citation impact, top 1% 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

190 citing papers in PubMed, 2 syntheses or guidelines pooled it, 295 citations in OpenAlex.

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  4. The mitochondrial chaperone HSPD1 folds MTHFD2 independently of its co-chaperone HSPE1.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
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130 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Lourdes Sainero-Alcolado *Department of Microbiology, Tumor and Cell Biology (MTC), Biomedicum B7, Karolinska Institutet, SE-171 65, Stockholm, Sweden.
Judit Liaño-Pons *Department of Microbiology, Tumor and Cell Biology (MTC), Biomedicum B7, Karolinska Institutet, SE-171 65, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-8097-4750
María Victoria Ruiz-PérezDepartment of Microbiology, Tumor and Cell Biology (MTC), Biomedicum B7, Karolinska Institutet, SE-171 65, Stockholm, Sweden.
Marie Arsenian-HenrikssonDepartment of Microbiology, Tumor and Cell Biology (MTC), Biomedicum B7, Karolinska Institutet, SE-171 65, Stockholm, Sweden. marie.arsenian.henriksson@ki.se.ORCID http://orcid.org/0000-0001-6376-7792
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During decades, the research field of cancer metabolism was based on the Warburg effect, described almost one century ago. Lately, the key role of mitochondria in cancer development has been demonstrated. Many mitochondrial pathways including oxidative phosphorylation, fatty acid, glutamine, and one carbon metabolism are altered in tumors, due to mutations in oncogenes and tumor suppressor genes, as well as in metabolic enzymes. This results in metabolic reprogramming that sustains rapid cell proliferation and can lead to an increase in reactive oxygen species used by cancer cells to maintain pro-tumorigenic signaling pathways while avoiding cellular death. The knowledge acquired on the importance of mitochondrial cancer metabolism is now being translated into clinical practice. Detailed genomic, transcriptomic, and metabolomic analysis of tumors are necessary to develop more precise treatments. The successful use of drugs targeting metabolic mitochondrial enzymes has highlighted the potential for their use in precision medicine and many therapeutic candidates are in clinical trials. However, development of efficient personalized drugs has proved challenging and the combination with other strategies such as chemocytotoxic drugs, immunotherapy, and ketogenic or calorie restriction diets is likely necessary to boost their potential. In this review, we summarize the main mitochondrial features, metabolic pathways, and their alterations in different cancer types. We also present an overview of current inhibitors, highlight enzymes that are attractive targets, and discuss challenges with translation of these approaches into clinical practice. The role of mitochondria in cancer is indisputable and presents several attractive targets for both tailored and personalized cancer therapy.

Indexed as

NeoplasmsPrecision MedicineHumansMitochondriaOxidative PhosphorylationReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID35831624
PMCPMC9287557
OpenAlexW4285084968

What OpenQuestion 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 OpenQuestion graph.