Converging protective pathways: Exploring the linkage between physical exercise, extracellular vesicles and oxidative stress

Lisi, Veronica; Senesi, Giorgia; Balbi, Carolina

doi:10.1016/j.freeradbiomed.2023.09.021

Cited by 5 publications

(1 citation statement)

References 139 publications

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“…Thus far, there is potential for skeletal muscle-derived miR-133a to target β-cell mitochondrial UCP2 and influence insulin secretion, given that an increase in skeletal muscle miR-133a leads to reduced UCP2 levels [190] and that β-cell UCP2 controls ROS production to promote GSIS [191]. Indeed, a marked rise in plasma EV protein content, especially antioxidant protein cargo (superoxide dismutase, catalase, and peroxiredoxin) is observed post-exercise to maintain a balanced redox state [192,193]. Currently it is unknown if EV-containing myokines influence pancreatic β-cell mitochondrial function and morphology within the context of prediabetes.…”

Section: Skeletal Muscle-derived Evs-islet β-Cell Crosstalkmentioning

confidence: 99%

Mitochondrial Dysfunction, Oxidative Stress, and Inter-Organ Miscommunications in T2D Progression

Veluthakal,

Esparza,

Hoolachan

et al. 2024

IJMS

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Type 2 diabetes (T2D) is a heterogenous disease, and conventionally, peripheral insulin resistance (IR) was thought to precede islet β-cell dysfunction, promoting progression from prediabetes to T2D. New evidence suggests that T2D-lean individuals experience early β-cell dysfunction without significant IR. Regardless of the primary event (i.e., IR vs. β-cell dysfunction) that contributes to dysglycemia, significant early-onset oxidative damage and mitochondrial dysfunction in multiple metabolic tissues may be a driver of T2D onset and progression. Oxidative stress, defined as the generation of reactive oxygen species (ROS), is mediated by hyperglycemia alone or in combination with lipids. Physiological oxidative stress promotes inter-tissue communication, while pathological oxidative stress promotes inter-tissue mis-communication, and new evidence suggests that this is mediated via extracellular vesicles (EVs), including mitochondria containing EVs. Under metabolic-related stress conditions, EV-mediated cross-talk between β-cells and skeletal muscle likely trigger mitochondrial anomalies leading to prediabetes and T2D. This article reviews the underlying molecular mechanisms in ROS-related pathogenesis of prediabetes, including mitophagy and mitochondrial dynamics due to oxidative stress. Further, this review will describe the potential of various therapeutic avenues for attenuating oxidative damage, reversing prediabetes and preventing progression to T2D.

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