Evidence map›Paper›PMID 39792183›Full record

ArticleCell biology and toxicology2025

Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.

Irene Gómez-Delgado, Andrea R López-Pastor, Adela González-Jiménez, Carlos Ramos-Acosta, Yenitzeh Hernández-Garate, Neus Martínez-Micaelo, Núria Amigó, Laura Espino-Paisán, Eduardo Anguita, Elena Urcelay

Abstract read
In one paragraph

Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Irene Gómez-Delgado *Lab. Genetics and Molecular Bases of Complex Diseases, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain.
Andrea R López-Pastor *Lab. Genetics and Molecular Bases of Complex Diseases, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain.
Adela González-JiménezLab. Genetics and Molecular Bases of Complex Diseases, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain.
Carlos Ramos-AcostaHematology Group, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain.
Yenitzeh Hernández-GarateLab. Genetics and Molecular Bases of Complex Diseases, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain.
Neus Martínez-MicaeloBiosfer Teslab, 43201, Reus, Tarragona, Spain.
Núria AmigóBiosfer Teslab, 43201, Reus, Tarragona, Spain.
Laura Espino-PaisánLab. Genetics and Molecular Bases of Complex Diseases, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain.
Eduardo Anguita *Hematology Group, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain.
Elena Urcelay *Lab. Genetics and Molecular Bases of Complex Diseases, Health Research Institute of Hospital Clínico San Carlos (IdISSC), 28040, Madrid, Spain. elena.urcelay@salud.madrid.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The underlying mechanisms explaining the differential course of SARS-CoV-2 infection and the potential clinical consequences after COVID-19 resolution have not been fully elucidated. As a dysregulated mitochondrial activity could impair the immune response, we explored long-lasting changes in mitochondrial functionality, circulating cytokine levels, and metabolomic profiles of infected individuals after symptoms resolution, to evaluate whether a complete recovery could be achieved. Results of this pilot study evidenced that different parameters of aerobic respiration in lymphocytes of individuals recuperated from a severe course lagged behind those shown upon mild COVID-19 recovery, in basal conditions and after simulated reinfection, and they also showed altered glycolytic capacity. The severe groups showed trends to enhanced superoxide production in parallel to lower OPA1-S levels. Unbalance of pivotal mitochondrial fusion (MFN2, OPA1) and fission (DRP1, FIS1) proteins was detected, suggesting a disruption in mitochondrial dynamics, as well as a lack of structural integrity in the electron transport chain. In serum, altered cytokine levels of IL-1β, IFN-α2, and IL-27 persisted long after clinical recovery, and growing amounts of the latter after severe infection correlated with lower basal and maximal respiration, ATP production, and glycolytic capacity. Finally, a trend for higher circulating levels of 3-hydroxybutyrate was found in individuals recovered after severe compared to mild course. In summary, long after acute infection, mitochondrial and metabolic changes seem to differ in a situation of full recovery after mild infection versus the one evolving from severe infection.

Indexed as

COVID-19CytokinesLymphocytesMitochondriaSARS-CoV-2AdultFemaleGlycolysisHumansMaleMiddle AgedMitochondrial DynamicsPilot ProjectsSeverity of Illness IndexCytokinesCOVID-19CytokinesDisease severityImmune systemMetabolomicsMitochondriaSARS-CoV-2

Identifiers

PMID39792183
PMCPMC11723900

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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.