Cited by 195Inflammasome and immune disordersAutophagy in Disease and TherapyMitochondrial Function and Pathology

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Mitochondrial dysfunction as a driver of NLRP3 inflammasome activation and its modulation through mitophagy for potential therapeutics

Mishra, Soumya Ranjan, Mahapatra, Kewal Kumar, Behera, Bishnu Prasad, Patra, Srimanta, Bhol, Chandra Sekhar, Panigrahi, Debasna Pritimanjari, Praharaj, Prakash Priyadarshi, Singh, Amruta, Patil, Shankargouda, Dhiman, Rohan, Bhutia, Sujit Kumar·2021·The International Journal of Biochemistry & Cell Biology

DOI 10.1016/j.biocel.2021.106013

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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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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: Mahapatra, Kewal Kumar
Behera, Bishnu Prasad
Patra, Srimanta
Bhol, Chandra Sekhar
Panigrahi, Debasna Pritimanjari
Praharaj, Prakash Priyadarshi
Singh, Amruta
Patil, Shankargouda
Dhiman, Rohan
Bhutia, Sujit Kumar
Venue: The International Journal of Biochemistry & Cell Biology
Publisher: Elsevier BV
Published: 2021-07
Volume: 136
Pages: 106013
ISSN: 1357-2725 (ISSN-L)
DOI: 10.1016/j.biocel.2021.106013
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: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
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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Mitochondrial dysfunction as a driver of NLRP3 inflammasome activation and its modulation through mitophagy for potential therapeutics

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