Cited by 3,479Mitochondrial Function and PathologyAutophagy in Disease and TherapyAdipose Tissue and Metabolism

Mitochondria: In Sickness and in Health

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Nunnari, Jodi, Suomalainen, Anu·2012·Cell

Abstract

Mitochondria perform diverse yet interconnected functions, producing ATP and many biosynthetic intermediates while also contributing to cellular stress responses such as autophagy and apoptosis. Mitochondria form a dynamic, interconnected network that is intimately integrated with other cellular compartments. In addition, mitochondrial functions extend beyond the boundaries of the cell and influence an organism's physiology by regulating communication between cells and tissues. It is therefore not surprising that mitochondrial dysfunction has emerged as a key factor in a myriad of diseases, including neurodegenerative and metabolic disorders. We provide a current view of how mitochondrial functions impinge on health and disease.

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Crossref · 10.1016/j.cell.2012.02.035

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243 of 243 references verified0 citation errors · 0 not checkable

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  • Detection of mitochondrial motives by innate and adaptive immunity might elicit potent pro-inflammatory responses.

    “Given the bacterial features of mitochondria, the detection of mitochondrial motives by cells of the innate and adaptive immunity might elicit potent pro-inflammatory responses147,276,277.”

    From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [277]

    The Introduction describes mitochondria’s bacterial ancestry, and “Mitochondrial Defects Cause Diverse and Complex Human Diseases” says that the innate immune system recognizes and targets mouse cells with allogenic mtDNA. Our copy does not say that adaptive immunity detects mitochondrial motifs or that such detection elicits potent pro-inflammatory responses. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • Mitochondria are the primary producers of intracellular reactive oxygen species and are susceptible to oxidative stress caused by toxic metabolites such as β-amyloid.

    “Mitochondria not only generate ATP but also act as the primary producers of intracellular reactive oxygen species (ROS) and are susceptible to oxidative stress caused by various toxic metabolites, such as β‐amyloid (Aβ) [3, 4].”

    From Aerobic exercise improves astrocyte mitochondrial quality and transfer to neurons in a mouse model of Alzheimer's disease (2025) · cites this paper as [3]

    The section “Mitochondria Are Metabolic Signaling Centers” states that mitochondrial complexes I and III generate ROS, and the paper also describes mitochondrial ATP production. It does not establish that mitochondria are the primary intracellular ROS producers or say that β-amyloid causes oxidative stress in mitochondria; searches for amyloid and Alzheimer-related oxidative stress did not find that link. Page numbers are unavailable in our copy. (LLM, conf=0.85)

    Experimental — accuracy not yet measured
  • MOMP eventually leads to the dissipation of the mitochondrial transmembrane potential (Δψm)-mostly as a consequence of the respiratory impairment imposed by the loss of CYCS-and hence to the cessation of Δψm-dependent mitochondrial functions (including ATP synthesis and some forms of protein import).

    “Of note, MOMP eventually leads to the dissipation of the mitochondrial transmembrane potential (Δψm)—mostly as a consequence of the respiratory impairment imposed by the loss of CYCS—and hence to the cessation of Δψm-dependent mitochondrial functions (including ATP synthesis and some forms of protein import) [200–203].”

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Authors
Nunnari, J., & Suomalainen, A.
Affiliations
  • University of California, Davis (US)
  • University of Helsinki (FI)
Corresponding author
  • Nunnari, Jodi
  • Suomalainen, Anu
Venue
Cell
Publisher
Elsevier BV
Published
2012-03
Volume
148
Issue
6
Pages
1145-1159
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2131415852
Cited by
3,479
References
243
Citations by year
2026: 290 · 2025: 372 · 2024: 418 · 2023: 313 · 2022: 316 · 2021: 292 · 2020: 277 · 2019: 213 · 2018: 193 · 2017: 182 · 2016: 163 · 2015: 150 · 2014: 147 · 2013: 108 · 2012: 43
FWCI
12.79
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Jane ja Aatos Erkon Säätiö
  • National Institutes of Health
  • National Institute of General Medical Sciences (R01GM062942, R01GM097432)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
mitochondria, mitochondrial dysfunction, ATP production, biosynthetic intermediates, autophagy, apoptosis, mitochondrial dynamics, intercellular communication, neurodegenerative diseases, metabolic disorders
MeSH terms
Animals, Autophagy, Humans, Mitochondria, Apoptosis, Neurodegenerative Diseases, Mitochondrial Diseases

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