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Peer-reviewedCC BY 4.0Molecules

Purinergic Signalling in Snakebite Envenomation: Mechanistic Insights, Therapeutic Targets and Future Perspectives

  • Dhébora Albuquerque Dias1
  • Maria Helena Souza Soares2
  • Rita de Cássia Avellaneda Guimarães3
  1. 1Laboratory of Food Physicochemical Analysis (LFQA), Faculty of Pharmaceutical Sciences, Food and Nutrition (FACFAN), Federal University of Mato Grosso do Sul (UFMS), Av. Costa e Silva s/n, Cidade Universitária, Campo Grande 79070-900, MS, Brazil
  2. 2Undergraduate Program in Food Engineering, Faculty of Pharmaceutical Sciences, Food and Nutrition (FACFAN), Federal University of Mato Grosso do Sul (UFMS), Av. Costa e Silva s/n, Cidade Universitária, Campo Grande 79070-900, MS, Brazil
  3. 3Graduate Program in Health and Development in the Central-West Region of Brazil, Medical School, Federal University of Mato Grosso do Sul (UFMS), Campo Grande 79070-900, MS, Brazil
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Abstract

Snakebite envenomation is a major neglected tropical disease associated with substantial morbidity and mortality. Its pathophysiology involves complex interactions between venom components and host responses, leading to inflammation, tissue damage, and systemic alterations. Purinergic signalling has emerged as an important mechanistic pathway underlying these processes. This narrative review was based on a comprehensive literature search of PubMed, Scopus, and Web of Science, focusing on purinergic signalling, snake venoms, inflammasome activation, extracellular nucleotide metabolism, and adjunct therapeutic strategies. Extracellular ATP, acting as a damage-associated molecular pattern (DAMP), activates purinergic receptors and amplifies inflammatory cascades, vascular dysfunction, and cell death pathways. CD39 and CD73 regulate extracellular nucleotide metabolism and generate adenosine, which exerts immunomodulatory and vascular effects. Venom-derived nucleotide-hydrolysing enzymes may also directly modulate host purinergic signalling, supporting an integrated network of host- and venom-derived mechanisms. Purinergic signalling represents a promising mechanistic target for adjunct therapy in snakebite envenomation; however, the temporal dynamics, efficacy, and safety of purinergic-targeted interventions require further preclinical and clinical validation.

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Cite

BibTeXRIS
BibTeX
@article{dias2026purinergic,
  title = {{Purinergic Signalling in Snakebite Envenomation: Mechanistic Insights, Therapeutic Targets and Future Perspectives}},
  author = {Dhébora Albuquerque Dias and Maria Helena Souza Soares and Rita de Cássia Avellaneda Guimarães},
  journal = {Molecules},
  year = {2026},
  month = oct,
  doi = {10.3390/molecules31203609},
  url = {https://www.mdpi.com/1420-3049/31/20/3609},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Purinergic Signalling in Snakebite Envenomation: Mechanistic Insights, Therapeutic Targets and Future Perspectives
AU  - Dhébora Albuquerque Dias
AU  - Maria Helena Souza Soares
AU  - Rita de Cássia Avellaneda Guimarães
PY  - 2026
DA  - 2026/10/10
JO  - Molecules
DO  - 10.3390/molecules31203609
UR  - https://www.mdpi.com/1420-3049/31/20/3609
AB  - Snakebite envenomation is a major neglected tropical disease associated with substantial morbidity and mortality. Its pathophysiology involves complex interactions between venom components and host responses, leading to inflammation, tissue damage, and systemic alterations. Purinergic signalling has emerged as an important mechanistic pathway underlying these processes. This narrative review was based on a comprehensive literature search of PubMed, Scopus, and Web of Science, focusing on purinergic signalling, snake venoms, inflammasome activation, extracellular nucleotide metabolism, and adjunct therapeutic strategies. Extracellular ATP, acting as a damage-associated molecular pattern (DAMP), activates purinergic receptors and amplifies inflammatory cascades, vascular dysfunction, and cell death pathways. CD39 and CD73 regulate extracellular nucleotide metabolism and generate adenosine, which exerts immunomodulatory and vascular effects. Venom-derived nucleotide-hydrolysing enzymes may also directly modulate host purinergic signalling, supporting an integrated network of host- and venom-derived mechanisms. Purinergic signalling represents a promising mechanistic target for adjunct therapy in snakebite envenomation; however, the temporal dynamics, efficacy, and safety of purinergic-targeted interventions require further preclinical and clinical validation.
SN  - 1420-3049
ER  -