Evidence map›Paper›PMID 40296438›Full record

ArticleEpilepsia open2025

Cardiac structural and molecular alterations in rodent models of temporal lobe epilepsy.

Zining Liu, Shobi Sivathamboo, Peravina Thergarajan, Flavia M Gomes, Idrish Ali, Kim L Powell, Piero Perucca, Nigel C Jones, Terence J O'Brien, Pablo Casillas-Espinosa

Abstract read
In one paragraph

Article in Epilepsia open, 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. 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

10 authors.

Zining LiuDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0002-5581-9270
Shobi SivathambooDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0003-4638-9579
Peravina ThergarajanDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.
Flavia M GomesDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.
Idrish AliDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0002-0971-4654
Kim L PowellDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0002-9007-4614
Piero PeruccaDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0002-7855-7066
Nigel C JonesDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0002-1080-8439
Terence J O'BrienDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.
Pablo Casillas-EspinosaDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0002-6199-9415

Funding

National Health and Medical Research Council of Australia APP1091593
6 · The paper itself

Abstract

objectiveCardiac structural and molecular changes are prevalent in people with chronic epilepsy, possibly contributing to an increased risk of premature mortality. However, understanding of the underlying pathophysiological mechanisms is limited. Here, we investigated the subacute and chronic changes in cardiac structure and ion channel/exchanger expression in different rodent models of temporal lobe epilepsy (TLE).

methodsTwo models of TLE were used: the kainic acid-induced post-status epilepticus (KASE) model in Wistar rats and the electrical self-sustained status epilepticus (SSSE) model in C57BL/6J mice. Heart tissue was collected at subacute (7 days post-SE) and chronic (12-16 weeks post-SE) timepoints from both models. Histological analysis for cardiac fibrosis and qPCR of ion channel/exchanger mRNA expression was performed.

resultsIncreased cardiac fibrosis was found in the KASE rats at the subacute (p = 0.016) and chronic (p = 0.003) timepoints compared with sham rats. In chronically epileptic KASE rats, mRNA expression analyses showed that Na SIGNIFICANCE: Cardiac alterations at structural and molecular levels were found in both experimental rodent epilepsy models, subacutely post-SE and during the chronically epileptic timepoint. The presence of similar cardiac changes across the models, despite being different species and having different modes of epilepsy indication, suggests that these changes are a direct or indirect result of the seizures. PLAIN LANGUAGE SUMMARY: Epilepsy may lead to heart problems, which could raise the risk of early death, but the exact causes are unclear. This study examined heart changes in two rodent models of epilepsy. In rats, heart scarring and stiffness (fibrosis) increased both shortly after seizures and during chronic epilepsy, and the ability to produce key heart proteins was altered. In mice, similar changes in heart proteins appeared in different heart areas. These findings suggest seizures can directly or indirectly cause harmful heart changes. Understanding these effects might help improve care for people with epilepsy and reduce related heart risks.

Indexed as

Epilepsy, Temporal LobeMyocardiumStatus EpilepticusAnimalsDisease Models, AnimalFibrosisKainic AcidMaleMiceMice, Inbred C57BLNAV1.5 Voltage-Gated Sodium ChannelRatsRats, WistarSodium-Calcium ExchangerKainic AcidNAV1.5 Voltage-Gated Sodium ChannelSodium-Calcium Exchangeranimal modelscardiac fibrosiscardiac hypertrophyion channelspost‐SE

Identifiers

PMID40296438
PMCPMC12163548

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Registered trials

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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.