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Updated: Mar 21, 2026

Author Spotlight: Oxygen-Independent Assays to Measure Mitochondrial Function in Mammals
Published on: May 19, 2023
Mitochondrial ROS regulation of proliferating cells
Lauren Diebold1, Navdeep S Chandel1
1Department of Medicine, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.
Abstract:
Once thought of exclusively as damaging molecules, reactive oxygen species (ROS) are becoming increasingly appreciated for the role they play in cellular signaling through redox biology. Notably, mitochondria are a major source of ROS within a cell (mROS). Mounting evidence now clearly shows that mROS are critical for intracellular redox signaling by which they contribute to a plethora of cellular processes such as proliferation. mROS are essential for physiological cell proliferation, particularly by the regulation of hypoxia inducible factors (HIFs) under hypoxia. mROS are also vital mediators of growth factor signaling cascades such as angiotensin II (Ang II) and T-cell receptor (TCR) signaling. Pathological proliferative diseases such as cancer utilize mROS to their advantage, aberrantly activating growth factor signaling cascades and perpetuating angiogenesis under hypoxia. This review discusses how mROS positively regulate mitogenic cellular signaling through redox biology, which is critical for both physiological and pathological proliferation.
Insights
Mitochondria-generated reactive oxygen species (ROS) are crucial for cell proliferation signaling. These molecules regulate both normal cell growth and the progression of diseases like cancer.
Area of Science:
- Redox biology
- Cellular signaling
- Mitochondrial function
Background:
- Reactive oxygen species (ROS) were traditionally viewed as damaging agents.
- Mitochondria are a primary source of intracellular ROS (mROS).
- Emerging evidence highlights mROS's critical role in cellular redox signaling.
Purpose of the Study:
- To review the positive regulatory role of mROS in mitogenic cellular signaling.
- To discuss the involvement of mROS in both physiological and pathological proliferation.
Main Methods:
- Literature review of studies on mROS and cellular proliferation.
- Analysis of mROS involvement in key signaling pathways (HIFs, Ang II, TCR).
- Examination of mROS's role in hypoxia and angiogenesis.
Main Results:
- mROS are essential for physiological cell proliferation, notably regulating hypoxia-inducible factors (HIFs).
- mROS mediate growth factor signaling cascades, including angiotensin II (Ang II) and T-cell receptor (TCR) pathways.
- Cancer cells exploit mROS to promote aberrant signaling, angiogenesis, and proliferation under hypoxia.
Conclusions:
- Mitochondrial ROS (mROS) are vital positive regulators of mitogenic signaling.
- Redox biology mediated by mROS is critical for normal cell proliferation.
- Aberrant mROS signaling contributes to pathological proliferative diseases, such as cancer.
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