Evidence map›Paper›PMID 34439778›Full record

ReviewBiomolecules2021

How Inflammation Pathways Contribute to Cell Death in Neuro-Muscular Disorders.

Sara Salucci, Anna Bartoletti Stella, Michela Battistelli, Sabrina Burattini, Alberto Bavelloni, Lucio Ildebrando Cocco, Pietro Gobbi, Irene Faenza

Abstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Observational
  2. Review
  3. Review
  4. Microglial reactivity predicts hippocampal, but not global, atrophy in cerebral small vessel disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Article
  6. Observational
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

8 authors.

Sara SalucciDepartment of Biomolecular Sciences (DiSB), Urbino University Carlo Bo, 61029 Urbino, Italy.ORCID 0000-0002-3507-4451
Anna Bartoletti StellaDepartment of Diagnostic Experimental and Specialty Medicine (DIMES), University of Bologna, 40126 Bologna, Italy.
Michela BattistelliDepartment of Biomolecular Sciences (DiSB), Urbino University Carlo Bo, 61029 Urbino, Italy.
Sabrina BurattiniDepartment of Biomolecular Sciences (DiSB), Urbino University Carlo Bo, 61029 Urbino, Italy.
Alberto BavelloniLaboratory of Experimental Oncology, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.ORCID 0000-0002-6467-1431
Lucio Ildebrando CoccoCellular Signalling Laboratory, Department of Biomedical and NeuroMotor Sciences (DIBINEM), University of Bologna, 40126 Bologna, Italy.ORCID 0000-0002-9206-8277
Pietro GobbiDepartment of Biomolecular Sciences (DiSB), Urbino University Carlo Bo, 61029 Urbino, Italy.ORCID 0000-0003-4705-0833
Irene FaenzaCellular Signalling Laboratory, Department of Biomedical and NeuroMotor Sciences (DIBINEM), University of Bologna, 40126 Bologna, Italy.ORCID 0000-0002-5227-3567

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuro-muscular disorders include a variety of diseases induced by genetic mutations resulting in muscle weakness and waste, swallowing and breathing difficulties. However, muscle alterations and nerve depletions involve specific molecular and cellular mechanisms which lead to the loss of motor-nerve or skeletal-muscle function, often due to an excessive cell death. Morphological and molecular studies demonstrated that a high number of these disorders seem characterized by an upregulated apoptosis which significantly contributes to the pathology. Cell death involvement is the consequence of some cellular processes that occur during diseases, including mitochondrial dysfunction, protein aggregation, free radical generation, excitotoxicity and inflammation. The latter represents an important mediator of disease progression, which, in the central nervous system, is known as neuroinflammation, characterized by reactive microglia and astroglia, as well the infiltration of peripheral monocytes and lymphocytes. Some of the mechanisms underlying inflammation have been linked to reactive oxygen species accumulation, which trigger mitochondrial genomic and respiratory chain instability, autophagy impairment and finally neuron or muscle cell death. This review discusses the main inflammatory pathways contributing to cell death in neuro-muscular disorders by highlighting the main mechanisms, the knowledge of which appears essential in developing therapeutic strategies to prevent the consequent neuron loss and muscle wasting.

Indexed as

ApoptosisAstrocytesAutophagyCytokinesDNA-Binding ProteinsGene Expression RegulationHereditary Sensory and Motor NeuropathyHumansInflammationMicrogliaMitochondriaMotor Neuron DiseaseMuscular DiseasesMuscular DystrophiesNeuromuscular Junction DiseasesNeuronsCytokinesDNA-Binding ProteinsNF-kappa BTARDBP protein, humancell deathinnate immune systemmotor neuron disordersneuroinflammationneuro-muscular diseases

Identifiers

PMID34439778
PMCPMC8391499

What OpenQuestion 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 OpenQuestion graph.