Implications of mitochondrial stress in a microgravity environment

Abstract

Introduction: Space travel is expected to become increasingly common. Although there is ongoing research on mitochondrial stress and its negative effects on the body, the impact of long-duration space missions is still not fully understood. Factors such as microgravity, radiation, and disrupted circadian rhythms can impair mitochondrial function, reduce ATP production, and increase reactive oxygen species (ROS), leading to metabolic and inflammatory consequences. Objective: to analyze and synthesize the available evidence on the effects of spaceflight-induced mitochondrial stress on target organs and its association with multisystem pathophysiological alterations. Methods: Narrative review based on a structured literature search in PubMed/MEDLINE and Google Scholar, including experimental, translational, and clinical studies published in English and Spanish. Evidence selection and synthesis were supported by the artificial intelligence tool Elicit, under critical manual review. Results: Microgravity induces complex mitochondrial adaptations, ranging from bioenergetic dysfunction to compensatory responses. Excess ROS and changes in mitochondrial morphology impair energy metabolism and contribute to bone, muscle, immune, and cardiovascular damage. However, methodological limitations prevent establishing definitive causal relationships. Conclusions: Mitochondria act as key mediators of damage induced by microgravity and cosmic radiation. Understanding these mechanisms will allow the development of strategies to reduce oxidative stress and preserve astronaut health during long-term missions. Longitudinal studies and more accurate models are needed to better define the balance between damage and adaptation.

Recibido: 27/11/2025

Aprobado: 04/02/2026