Evidence map›Paper›PMID 40694302›Full record

ArticleCell biochemistry and biophysics2025

Pathological Changes in Liver Mitochondria of Rats with Experimentally Induced Hyperthyroidism and Their Correction with Uridine.

Natalya Venediktova, Natalya Khmil, Lyubov Pavlik, Irina Mikheeva, Galina Mironova

Abstract read
PubMed Publisher
In one paragraph

Article in Cell biochemistry and biophysics, 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. Review
  2. Article
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

5 authors.

Natalya VenediktovaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia. tiggra4@yandex.ru.
Natalya KhmilInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.
Lyubov PavlikInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.
Irina MikheevaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.
Galina MironovaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the study was to examine how the administration of uridine influences the mitochondrial function in hepatocytes in a rat model of hyperthyroidism (HT) induced by thyroxine treatment. Excess thyroid hormones (TH) increased the mitochondrial oxygen consumption, enhanced biogenesis, and altered the expression of proteins regulating the mitochondrial fusion and fission. Hyperthyroid rats had a mixed population of mitochondria, including swollen and damaged organelles. Although uridine did not affect the level of serum TH, it restored the normal body weight. The administration of uridine used for therapeutic purposes improved the main parameters of respiration and oxidative phosphorylation, prevented destructive changes in the morphology of liver mitochondria, and influenced the biogenesis and dynamics of these organelles. Overall, the results obtained indicate that uridine has a protective effect against functional and some structural destructions in rat liver mitochondria induced by HT.

Indexed as

HyperthyroidismMitochondria, LiverUridineAnimalsMaleMitochondrial DynamicsOxidative PhosphorylationOxygen ConsumptionRatsRats, WistarThyroid HormonesThyroxineThyroid HormonesThyroxineUridineETC dysfunctionLiver metabolismliver mitochondriaT3/T4 homeostasisUridine

Identifiers

What Socratic 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 Socratic graph.