Evidence mapPaperPMID 39495479Full record

ArticleGeroScience2025

Novel biomarkers of mitochondrial dysfunction in Long COVID patients.

Titanilla Szögi, Barbara N Borsos, Dejana Masic, Bence Radics, Zsolt Bella, Andrea Bánfi, Nóra Ördög, Csenge Zsiros, Ágnes Kiricsi, Gabriella Pankotai-Bodó and 10 more

Abstract read
In one paragraph

Article in GeroScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

20 authors.

Titanilla SzögiDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Barbara N BorsosDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Dejana MasicDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Bence RadicsDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Zsolt BellaDepartment of Oto-Rhino- Laryngology and Head-Neck Surgery, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Andrea BánfiDepartment of Pediatrics and Pediatric Health Center, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Nóra ÖrdögDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Csenge ZsirosDepartment of Oto-Rhino- Laryngology and Head-Neck Surgery, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Ágnes KiricsiDepartment of Oto-Rhino- Laryngology and Head-Neck Surgery, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Gabriella Pankotai-BodóDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Ágnes KovácsPulmonology Clinic, Albert Szent-Györgyi Medical and Pharmaceutical Centre, University of Szeged, Szeged, Hungary.
Dóra ParóczaiDepartment of Internal Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Andrea Lugosi BotkánéPulmonology Clinic, Albert Szent-Györgyi Medical and Pharmaceutical Centre, University of Szeged, Szeged, Hungary.
Béla KajtárDepartment of Pathology, University of Pécs Medical School, Pécs, Hungary.
Farkas SükösdDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Andrea LehoczkiDoctoral College, Health Sciences Program, Semmelweis University, Budapest, Hungary.
Tamás PolgárInstitute of Biophysics, HUN-REN Biological Research Centre, Szeged, Hungary.
Annamária LetohaDepartment of Internal Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Tibor Pankotai *Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary. pankotai.tibor@szte.hu.ORCID 0000-0001-9810-5465
László Tiszlavicz *Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.

Funding

Horizon 2020 Framework Programme 739593Magyar Tudományos Akadémia POST-COVID2021-36Nemzeti Kutatási, Fejlesztési és Innovaciós Alap 2022-2.1.1-NL-2022-00005Nemzeti Kutatási, Fejlesztési és Innovaciós Alap TKP-2021-EGA-05Nemzeti Kutatási, Fejlesztési és Innovaciós Alap TKP2021-NKTA-47Nemzeti Kutatási Fejlesztési és Innovációs Hivatal NKFI-FK 132080Nemzeti Kutatási Fejlesztési és Innovációs Hivatal RRF-2.3.1-21-2022-00003
6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) can lead to severe acute respiratory syndrome, and while most individuals recover within weeks, approximately 30-40% experience persistent symptoms collectively known as Long COVID, post-COVID-19 syndrome, or post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (PASC). These enduring symptoms, including fatigue, respiratory difficulties, body pain, short-term memory loss, concentration issues, and sleep disturbances, can persist for months. According to recent studies, SARS-CoV-2 infection causes prolonged disruptions in mitochondrial function, significantly altering cellular energy metabolism. Our research employed transmission electron microscopy to reveal distinct mitochondrial structural abnormalities in Long COVID patients, notably including significant swelling, disrupted cristae, and an overall irregular morphology, which collectively indicates severe mitochondrial distress. We noted increased levels of superoxide dismutase 1 which signals oxidative stress and elevated autophagy-related 4B cysteine peptidase levels, indicating disruptions in mitophagy. Importantly, our analysis also identified reduced levels of circulating cell-free mitochondrial DNA (ccf-mtDNA) in these patients, serving as a novel biomarker for the condition. These findings underscore the crucial role of persistent mitochondrial dysfunction in the pathogenesis of Long COVID. Further exploration of the cellular and molecular mechanisms underlying post-viral mitochondrial dysfunction is critical, particularly to understand the roles of autoimmune reactions and the reactivation of latent viruses in perpetuating these conditions. This comprehensive understanding could pave the way for targeted therapeutic interventions designed to alleviate the chronic impacts of Long COVID. By utilizing circulating ccf-mtDNA and other novel mitochondrial biomarkers, we can enhance our diagnostic capabilities and improve the management of this complex syndrome.

Indexed as

COVID-19MitochondriaMitochondrial DiseasesAgedBiomarkersDNA, MitochondrialFemaleHumansMaleMicroscopy, Electron, TransmissionMiddle AgedOxidative StressPost-Acute COVID-19 SyndromeSARS-CoV-2BiomarkersDNA, MitochondrialMitochondriaMitophagymtDNAOxidative damagePost-COVID

Identifiers

PMID39495479
PMCPMC11979091

What Socratic holds

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LicenceCC BY
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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.