Endothelial progenitor cells repairing damaged lung tissue

Can Endothelial Progenitor Cells Rescue Damaged Lungs?

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Avery Sinclair in Health & Wellness December 2025 • 4 min read.

"Exploring new frontiers in acute lung injury treatment."


Acute lung injury (ALI) remains a critical healthcare challenge, spurring the search for innovative treatments. Among these, endothelial progenitor cells (EPCs) have emerged as promising therapeutic agents. First identified in 1997, these cells offer potential in treating various diseases, including ALI, by aiding in tissue repair and reducing inflammation.

EPCs, derived from bone marrow, are characterized as CD34+/VEGFR2+/CD133+ cells. Their primary function involves repairing damaged vascular endothelium and promoting new blood vessel formation. This is achieved through direct differentiation into endothelial cells and the release of paracrine signals, such as vascular endothelial growth factor (VEGF) and stromal derived factor-1 (SDF-1).

Additionally, EPCs play a crucial role in modulating inflammatory responses by suppressing interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), toll-like receptor 4, and IL-6. Recent studies have also highlighted the role of EPC-produced exosomes, containing microRNA (like miR-126), in alleviating lung injury. These findings suggest EPCs could offer a novel approach to managing lung inflammation and damage.

How EPCs Could Combat Respiratory Distress

Endothelial progenitor cells repairing damaged lung tissue

Acute respiratory distress syndrome (ARDS) arises from widespread lung injury, leading to respiratory failure. Characterized by neutrophil influx and subsequent pro-inflammatory cascades, ARDS results in significant epithelial and endothelial damage. Despite medical advances, ARDS mortality remains high, underscoring the need for more effective treatments.

Cell-based therapies, particularly mesenchymal stromal cells (MSCs), have gained attention as potential ARDS treatments. Pre-clinical studies indicate that MSCs can reduce inflammation and improve survival rates in animal models and explanted human lungs. However, clinical trial results for systemic MSC administration in ARDS are still limited.

  • EPCs in Focus: While MSCs show promise, EPCs also hold significant potential. They remain attractive as possible therapeutic agents for ARDS and sepsis, backed by supportive data from mouse models.
  • Survival Link: Intriguingly, circulating EPC levels correlate with survival rates in ARDS patients, suggesting their therapeutic relevance.
  • Journal Insights: A study by Mao et al. explores how EPCs protect against endotoxin-induced lung injury in mice, revealing their direct inhibitory effects on neutrophils.
The co-culture of EPCs with neutrophils demonstrated a reduction in inflammatory cytokines (IL-1β and TNF-α) and tissue-destructive enzymes, such as neutrophil elastase (NE) and matrix metalloproteinase-9 (MMP9). These findings align with previous results showing decreased lung injury scores and histological improvements.

The Future of EPCs in Lung Injury Treatment

While research indicates EPCs can attenuate lung injury by reducing inflammation and tissue damage, questions remain regarding their precise mechanisms of action. Specifically, whether these effects are mediated through paracrine signaling or direct cell-cell interaction needs further exploration.

The current research focuses on systemic endotoxin-induced lung injury without infection. Future studies should assess EPC effects in models that mimic clinical sepsis more closely, including bacterial infections and direct airway endotoxin administration. Understanding EPCs' effects on neutrophils and other inflammatory pathways is crucial for advancing their therapeutic application.

In summary, EPCs show promise for treating ARDS, potentially by leveraging their anti-inflammatory properties. Despite encouraging pre-clinical results, clinical trials are needed to confirm their efficacy in ARDS and sepsis. Further research elucidating how EPCs modulate neutrophil behavior in vitro and in vivo will pave the way for translating these findings into effective bedside treatments.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1016/j.amjms.2018.10.002, Alternate LINK

Title: Acute Lung Injury: Endothelial Progenitor Cells To The Rescue?

Subject: General Medicine

Journal: The American Journal of the Medical Sciences

Publisher: Elsevier BV

Authors: Viranuj Sueblinvong, Daniel J. Weiss

Published: 2019-01-01

Everything You Need To Know

1

What exactly are Endothelial Progenitor Cells (EPCs)?

Endothelial progenitor cells (EPCs) are cells derived from bone marrow and are characterized as CD34+/VEGFR2+/CD133+ cells. They are crucial for repairing damaged vascular endothelium and promoting new blood vessel formation. This is achieved through direct differentiation into endothelial cells and the release of paracrine signals, such as vascular endothelial growth factor (VEGF) and stromal derived factor-1 (SDF-1). Their ability to combat lung injury makes them a promising therapeutic agent.

2

What is Acute Lung Injury (ALI) and why is it important?

Acute lung injury (ALI) is a critical healthcare challenge and respiratory distress syndrome (ARDS) is one of its severest manifestations. ARDS arises from widespread lung injury, leading to respiratory failure, characterized by neutrophil influx and subsequent pro-inflammatory cascades, resulting in significant epithelial and endothelial damage. Given that ARDS mortality remains high, exploring innovative treatments like EPCs is vital.

3

Why are Endothelial Progenitor Cells (EPCs) so significant in the context of lung injury?

EPCs are significant because they have the potential to revolutionize the treatment of acute lung injury (ALI) and related respiratory distress syndromes. They aid in tissue repair, reduce inflammation, and promote new blood vessel formation. Studies, like the one by Mao et al., have shown EPCs' direct inhibitory effects on neutrophils, and their ability to reduce inflammatory cytokines and tissue-destructive enzymes. Circulating EPC levels correlate with survival rates in ARDS patients, making them an attractive therapeutic option.

4

How do Endothelial Progenitor Cells (EPCs) help combat respiratory distress?

EPCs combat respiratory distress by several mechanisms. First, they repair damaged vascular endothelium and promote new blood vessel formation, which is crucial for lung function. Second, they modulate inflammatory responses by suppressing interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), toll-like receptor 4, and IL-6. Further, EPC-produced exosomes, containing microRNA (like miR-126), can alleviate lung injury. These combined effects make EPCs a potent agent in managing lung inflammation and damage.

5

What are the implications of using Endothelial Progenitor Cells (EPCs) in treating lung injury?

The implications of using EPCs include a novel approach to managing lung inflammation and damage, potentially offering a more effective treatment for conditions like Acute respiratory distress syndrome (ARDS) where traditional methods fall short. The use of EPCs could significantly improve survival rates and outcomes for patients suffering from these critical respiratory illnesses. Further research is needed to explore the precise mechanisms of action of EPCs and to understand whether these effects are mediated through paracrine signaling or direct cell-cell interaction.

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