International journal of molecular sciencesMay 13, 2026

Mitochondria as a Central Controller of Cell Balance and Stress Response

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated May 14, 2026

Abstract

Mitochondrial dysfunction is linked to diverse disorders, including rheumatoid arthritis, ischemic stroke, and autism spectrum disorder.

Mitochondria play crucial roles in energy production and regulating cellular responses to stress.
Disruption of mitochondrial quality control mechanisms can lead to disease initiation and progression.
Common mitochondrial abnormalities across rheumatoid arthritis, ischemic stroke, and autism spectrum disorder include metabolic reprogramming toward glycolysis and impaired removal of damaged organelles.
In rheumatoid arthritis, mitochondrial dysfunction contributes to chronic inflammation and joint damage.
In ischemic stroke, acute mitochondrial failure and oxidative stress are associated with neuronal injury.
In autism spectrum disorder, mitochondrial metabolic inflexibility may lead to chronic inflammation and neurodevelopmental challenges.

Simplified

Mitochondria are increasingly recognized as multifunctional organelles that integrate metabolic, redox, immune, and cell fate signaling, thereby maintaining cellular and tissue homeostasis under physiological conditions. Beyond their classical role in ATP production, mitochondria act as central regulatory hubs coordinating adaptive responses to metabolic demands and environmental stress. These functions are sustained through tightly regulated quality control mechanisms, including mitochondrial biogenesis, dynamic fusion-fission remodeling, redox signaling, and selective removal of damaged organelles via mitophagy. Disruption of these processes compromises cellular resilience and contributes to disease initiation and progression. This review summarizes and critically evaluates current evidence on mitochondrial function in health and its dysregulation in pathological conditions, with a particular focus on rheumatoid arthritis (RA), ischemic stroke (IS), and autism spectrum disorder (ASD). Despite their distinct clinical manifestations, these disorders share convergent mitochondrial abnormalities, including metabolic reprogramming toward glycolysis, excessive or persistent reactive oxygen species production, impaired mitophagy, mitochondrial DNA-driven innate immune activation, and hypoxia-related stress. In RA, mitochondrial dysfunction sustains chronic inflammation and joint destruction; in IS, acute mitochondrial failure and reperfusion-associated oxidative stress drive neuronal injury; and in ASD, mitochondrial metabolic inflexibility and defective quality control contribute to chronic low-grade inflammation and neurodevelopmental vulnerability. A variety of methods for the assessment of mitochondrial function are available to study these pathological conditions. Collectively, these findings position mitochondrial dysfunction as a unifying pathogenic mechanism linking inflammatory, neurodegenerative, and neurodevelopmental processes. Targeting mitochondrial metabolism, redox balance, and quality control pathways therefore represents a promising cross-disease therapeutic strategy.

Funding

Competing interests

The authors report there are no conflicts of interest concerning this article.

PubMed

Mitochondria as a Central Controller of Cell Balance and Stress Response

Abstract

Funding

Competing interests

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Abstract

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