Evidence map›Paper›PMID 34472002›Full record

ReviewMolecular and cellular biochemistry2021

Mitochondrial dysfunction in perinatal asphyxia: role in pathogenesis and potential therapeutic interventions.

Puneet K Samaiya, Sairam Krishnamurthy, Ashok Kumar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Inflammatory mechanisms contribute to long-term cognitive deficits induced by perinatal asphyxia via interleukin-1.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Effects ofHuman reproduction open · 2024
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. 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

3 authors at 3 institutions in 1 country.

Puneet K SamaiyaDepartment of Pharmacy, Shri G.S. Institute of Technology and Science, Indore, MP, 452003, India. punit.samaiya@gmail.com.ORCID http://orcid.org/0000-0001-7836-8807
Sairam KrishnamurthyNeurotherapeutics Lab, Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, 221005, India.
Ashok KumarDepartment of Pediatrics, Institute of Medical Sciences, BHU, Varanasi, UP, India.
Banaras Hindu University · INIndian Institute of Technology Indore · INInstitute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perinatal asphyxia (PA)-induced brain injury may present as hypoxic-ischemic encephalopathy in the neonatal period, and long-term sequelae such as spastic motor deficits, intellectual disability, seizure disorders and learning disabilities. The brain injury is secondary to both the hypoxic-ischemic event and oxygenation-reperfusion following resuscitation. Following PA, a time-dependent progression of neuronal insult takes place in terms of transition of cell death from necrosis to apoptosis. This transition is the result of time-dependent progression of pathomechanisms which involve excitotoxicity, oxidative stress, and ultimately mitochondrial dysfunction in developing brain. More precisely mitochondrial respiration is suppressed and calcium signalling is dysregulated. Consequently, Bax-dependent mitochondrial permeabilization occurs leading to release of cytochrome c and activation of caspases leading to transition of cell death in developing brain. The therapeutic window lies within this transition process. At present, therapeutic hypothermia (TH) is the only clinical treatment available for treating moderate as well as severe asphyxia in new-born as it attenuates secondary loss of high-energy phosphates (ATP) (Solevåg et al. in Free Radic Biol Med 142:113-122, 2019; Gunn et al. in Pediatr Res 81:202-209, 2017), improving both short- and long-term outcomes. Mitoprotective therapies can offer a new avenue of intervention alone or in combination with therapeutic hypothermia for babies with birth asphyxia. This review will explore these mitochondrial pathways, and finally will summarize past and current efforts in targeting these pathways after PA, as a means of identifying new avenues of therapeutic intervention.

Indexed as

AnimalsAsphyxia NeonatorumFemaleHumansHypothermia, InducedHypoxia-Ischemia, BrainInfant, NewbornMitochondriaNeuroprotective AgentsOxidative StressPregnancyNeuroprotective AgentsApoptosisApoptosomeExcitotoxicityHypoxic-ischemic encephalopathyMitochondriaPerinatal asphyxia

Identifiers

PMID34472002
OpenAlexW3197978476

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.