Evidence map›Paper›PMID 40682648›Full record

ArticleBulletin of experimental biology and medicine2025

Age-Dependent Changes in Mitochondrial Regulatory Mechanisms in the Spinal Cord of SOD1-G93A-Transgenic Mice with the Phenotype of Amyotrophic Lateral Sclerosis.

N V Belosludtseva, I B Mikheeva, V S Starinets, M V Dubinin, K N Belosludtsev

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Article in Bulletin of experimental biology and medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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.

N V BelosludtsevaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia. nata.imagination@gmail.com.
I B MikheevaInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.
V S StarinetsInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.
M V DubininMari State University, Yoshkar-Ola, , Mari El Republic, Russia.
K N BelosludtsevInstitute 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

Age-dependent changes in the expression level of genes encoding proteins responsible for mitochondrial homeostasis were studied in relation to ultrastructural abnormalities in the mitochondria of motor neurons in the anterior horns of the spinal cord in a transgenic model of amyotrophic lateral sclerosis (SOD1-G93A mice). The expression of the Drp1, Mfn2, Ppargc1a, and Nefl genes was reduced, and the expression of the Nfe2l2, Pink1, and Parkin genes was enhanced in mice with the genotype of the familial form of the disease at the age of 22 weeks corresponding to the symptomatic stage in comparison with wild-type mice (C57BL6 × SJL) and non-transgenic littermates (SOD1-G93A(Tg-)) of the same age. Comparative analysis of spinal cord tissue samples from 8 and 12 weeks-old animals revealed no significant differences in the expression levels of genes encoding proteins responsible for mitochondrial dynamics, biogenesis, and mitophagy. Electron microscopic examination showed pronounced structural alterations in mitochondria in the soma of lower motor neurons of SOD1-G93A(Tg+) mice at the symptomatic stage, which manifested in the appearance of "ring-like" mitochondrial structures, matrix swelling, destruction of membranes in the cristae, and increased number of autophagolysosomes. The role of mitochondrial homeostasis disorders in the progression of amyotrophic lateral sclerosis is discussed.

Indexed as

Amyotrophic Lateral SclerosisMitochondriaSpinal CordSuperoxide Dismutase-1AnimalsDisease Models, AnimalDynaminsGTP PhosphohydrolasesHumansMaleMiceMice, Inbred C57BLMice, TransgenicMitochondrial DynamicsMitochondrial ProteinsMitophagyDnm1l protein, mouseDynaminsGTP PhosphohydrolasesMfn2 protein, mouseMitochondrial ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2parkin proteinPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseProtein KinasesPTEN-Induced Putative KinaseSOD1 G93A proteinSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Ubiquitin-Protein Ligasesamyotrophic lateral sclerosislower motor neuronsmitochondrial biogenesismitochondrial dynamicsspinal cord

Identifiers

PMID40682648

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