Evidence mapPaperPMID 40879880Full record

ReviewMetabolic brain disease2025

Microglial pyroptosis in neurological disorders: mechanistic crosstalk, metabolic triggers, and therapeutic frontiers.

Reetesh Kumar, Siva Parsad Panda, Mosleh Mohammad Abomughaid, Sorabh Lakhanpal, D Avinash, Niraj Kumar Jha, Rohan Gupta

Abstract readReview
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In one paragraph

Review in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. MIF Tautomerase Inhibition Protects Neurons From Immune-Mediated Cell Death.Neurology(R) neuroimmunology & neuroinflammation · 2026
    Article
  4. Review
  5. Review
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

7 authors.

Reetesh KumarDepartment of Bioengineering and Biotechnology, School of Biosciences & Technology, Galgotias University, Greater Noida, 203201, Uttar Pradesh, India.
Siva Parsad PandaInstitute of Pharmaceutical Research, GLA University, Mathura, 281406, Uttar Pradesh, India.
Mosleh Mohammad AbomughaidDepartment of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Bisha, Bisha, 61922, Saudi Arabia.
Sorabh LakhanpalSchool of Pharmaceutical Sciences, Lovely Professional University, Phagwara, 144411, Punjab, India.
D AvinashCenter for Global Health Research, Saveetha Medical College, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.
Niraj Kumar JhaDepartment of Bioengineering and Biotechnology, School of Biosciences & Technology, Galgotias University, Greater Noida, 203201, Uttar Pradesh, India.ORCID 0000-0001-9486-4069
Rohan GuptaDepartment of Bioengineering and Biotechnology, School of Biosciences & Technology, Galgotias University, Greater Noida, 203201, Uttar Pradesh, India. rohan.gupta@galgotiasuniversity.edu.in.ORCID 0000-0002-6635-6558

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases (NDDs) are characterized by the progressive decline of neuronal structure and function, with neuroinflammation and neuronal death as key pathogenic features. Pyroptosis, a highly inflammatory kind of programmed cell death (PCD) facilitated by gasdermin (GSDM) proteins and inflammasome activation, has garnered significant attention among new mechanisms. The increased expression of pyroptosis-related proteins, frequently co-localized with misfolded protein aggregates, indicates a crucial involvement in the advancement of different NDDs. Further, microglial pyroptosis exacerbates neuronal damage by hindering the removal of neurotoxic chemicals and intensifying inflammatory responses. Epigenetic and post-translational modifications (PTMs) of histone and non-histone proteins, along with metabolic dysregulation, significantly influence pyroptotic signaling, ultimately expediting neurodegeneration. Pyroptosis, owing to its pivotal involvement in inflammation and neuronal demise, is gaining recognition as a possible diagnostic and prognostic biomarker, particularly in the advancement of immunotherapeutic approaches. Herein, we thoroughly examine the molecular control of pyroptosis through PTMs and metabolic pathways, its implications for neurodegenerative and neuropsychiatric disorders, and recent therapeutic developments aimed at targeting pyroptotic pathways. It emphasizes the advancement of novel diagnostic instruments, such as genetic reporters and nanomaterial-based molecular probes for the real-time and non-invasive identification of pyroptotic activity. These discoveries establish a foundation for future tailored treatment strategies designed to alleviate pyroptosis-induced neuroinflammation and neurodegeneration. HIGHLIGHTS: 1. Pyroptosis is a pro-inflammatory cell death linked to neuroinflammatory conditions. 2. ROS and oxidative stress connect pyroptosis with other cell death mechanisms. 3. Altered glucose and lipid metabolism influence pyroptosis and neuronal degeneration. 4. PTMs of GSDMD, caspase-1, and ASC regulate pyroptosis in brain disorders. 5. Targeting microglial pyroptosis offers potential therapy for neurodegenerative diseases.

Indexed as

MicrogliaNervous System DiseasesNeurodegenerative DiseasesPyroptosisAnimalsHumansInflammasomesInflammasomesDetection techniquesMetabolic regulationNeurodegenerative diseasesPost-translational modificationsPyroptosisTherapeutics

Identifiers

What Socratic holds

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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.