The DOI matches its Crossref record; 82 of the 84 references it cites were found in a registry or an index.
Mitochondrial dysfunction as a driver of NLRP3 inflammasome activation and its modulation through mitophagy for potential therapeutics
Abstract
The NLR family pyrin domain containing 3 (NLRP3) inflammasome is responsible for the sensation of various pathogenic and non-pathogenic damage signals and has a vital role in neuroinflammation and neural diseases. Various stimuli, such as microbial infection, misfolded protein aggregates, and aberrant deposition of proteins can induce NLRP3 inflammasome in neural cells. Once triggered, the NLRP3 inflammasome leads to the activation of caspase-1, which in turn activates inflammatory cytokines, such as interleukin-1β and interleukin -18, and induces pyroptotic cell death. Mitochondria are critically involved in diverse cellular processes and are involved in regulating cellular redox status, calcium levels, inflammasome activation, and cell death. Mitochondrial dysfunction and subsequent accumulation of mitochondrial reactive oxygen species, mitochondrial deoxyribonucleic acid, and other mitochondria-associated proteins and lipids play vital roles in the instigation of the NLRP3 inflammasome. In addition, the processes of mitochondrial dynamics, such as fission and fusion, are essential in the maintenance of mitochondrial integrity and their imbalance also promotes NLRP3 inflammasome activation. In this connection, mitophagy-mediated maintenance of mitochondrial homeostasis restricts NLRP3 inflammasome hyperactivation and its consequences in various neurological disorders. Hence, mitophagy can be exploited as a potential strategy to target damaged mitochondria induced NLRP3 inflammasome activation and its lethal consequences. Therefore, the identification of novel mitophagy modulators has promising therapeutic potential for NLRP3 inflammasome-associated neuronal diseases.
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“ROS increase with age due to mitochondrial dysfunction and inflammation, and can also drive NLRP3 inflammasome activation, likely further contributing to COVID-19 pathophysiology in the elderly58,76,77.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [77]
Citations
Cites
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Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores
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Cited by
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Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances
Xu, X., Pang, Y., & Fan, X. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02253-4 · Cited by 975
SARS-CoV-2, COVID-19 and the aging immune system
Bartleson, J. M., Radenkovic, D., Covarrubias, A. J., Furman, D., Winer, D. A., & Verdin, E. (2021) · Nature Aging · doi:10.1038/s43587-021-00114-7 · Cited by 359
Exploring the Role of Neuroplasticity in Development, Aging, and Neurodegeneration
Marzola, P., Melzer, T., Pavesi, E., Gil-Mohapel, J., & Brocardo, P. S. (2023) · Brain Sciences · doi:10.3390/brainsci13121610 · Cited by 281
Riegger, J., Schoppa, A., Ruths, L., Haffner‐Luntzer, M., & Ignatius, A. A. (2023) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-023-00489-y · Cited by 261
The Role of NLRP3 Inflammasome in Alzheimer’s Disease and Potential Therapeutic Targets
Liang, T., Zhang, Y., Wu, S., Chen, Q., & Wang, L. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.845185 · Cited by 226
Metadata
- Authors
- Mishra, S. R., Mahapatra, K. K., Behera, B. P., Patra, S., Bhol, C. S., Panigrahi, D. P., Praharaj, P. P., Singh, A., Patil, S., Dhiman, R., & Bhutia, S. K.
- Affiliations
- National Institute of Technology Rourkela (IN)
- Jazan University (SA)
- Corresponding author
- Bhutia, Sujit Kumar
- ORCID
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2021-07
- Volume
- 136
- Pages
- 106013
- ISSN
- 1357-2725 (ISSN-L)
- OpenAlex
- W3161796677
- Semantic Scholar
- b4a92ba89affa9b84a67beeda34ec1a57be1bd99
- Cited by
- 195
- References
- 84
- Citations by year
- 2026: 51 · 2025: 47 · 2024: 37 · 2023: 27 · 2022: 29 · 2021: 4
- FWCI
- 2.55
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Department of Biotechnology
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- NLRP3 inflammasome, mitochondrial dysfunction, mitophagy, neuroinflammation, pyroptosis, caspase-1, IL-1β, IL-18, mitochondrial dynamics, mitochondrial reactive oxygen species, mitochondrial DNA, mitochondrial homeostasis, neurodegenerative diseases
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Humans, Inflammation, Mitochondria, Mitochondrial Proteins, Inflammasomes, Mitochondrial Dynamics, Mitophagy
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