# Redox Regulation of Complement Pathway Activation in Aging and Related Diseases

## TL;DR

This review explains how oxidative stress and the immune system's complement pathway work together to worsen aging and related diseases, and how targeting this interaction could help promote healthier aging.

## Contribution

The paper highlights the underappreciated interplay between oxidative stress and the complement system in aging and disease.

## Key findings

- Redox imbalance activates complement components, which in turn amplify oxidative stress, creating a harmful cycle.
- This redox–complement axis plays a key role in the progression of neurodegenerative, cardiovascular, and metabolic diseases.
- Therapeutic strategies targeting this interaction show promise for disrupting the cycle and improving health outcomes.

## Abstract

Aging is a complex degenerative process characterized by the accumulation of molecular damage and a heightened susceptibility to disease. The oxidative stress theory of aging identifies endogenous reactive oxygen species (ROS) as primary drivers of this cellular deterioration. This review provides a comprehensive analysis of the critical, yet underappreciated, interplay between oxidative stress and the complement system, a powerful effector of innate immunity. We detail the mechanistic pathways through which redox imbalance directly activates complement components and, conversely, how complement activation amplifies oxidative stress, creating a vicious cycle that accelerates tissue damage. A central focus is placed on how this redox–complement axis contributes to the pathophysiology of age-related conditions, including neurodegenerative, cardiovascular, and metabolic diseases. Furthermore, the review explores emerging therapeutic strategies that target this interaction, highlighting the potential of antioxidant and complement-inhibitory approaches to disrupt this cycle and promote healthy aging. By synthesizing current evidence, this work underscores the significance of the redox–complement network as a key mechanistic link in aging and its associated diseases.