Stem Cells: The Cellular Origins of Fibrosis - European Medical Journal

Stem Cells: The Cellular Origins of Fibrosis

1 Mins
General Healthcare

POTENTIAL culprits that give rise to chronic tissue scarring, which can lead to the development of fibrosis, have been identified as a rare population of stem cells (SCs). Tissue scarring caused by organ damage is associated with a multitude of health conditions such as: diabetes, lung disease, high blood pressure (HBP), and kidney disease.

Worryingly, it is estimated that fibrosis contributes to a staggering 45% of all deaths in the developed world. Inflammation and reduced blood and oxygen delivery to the organs are the main damaging consequences of fibrosis. The progressive development of scar tissue can lead to organ failure and death. Researchers found, in mice models, that a rare population of SCs located outside of blood vessels become myofibroblast cells that secrete proteins, causing scar tissue.

“Under normal circumstances, myofibroblasts stimulate wound healing, but when there is an ongoing injury to an organ (e.g. the liver of a hepatitis C patient, the heart of a patient with HBP, or the kidney of a patient with diabetes) these proteins clog up normal functioning,” said Dr Benjamin Humphreys, Director of the Harvard Stem Cell Institute Kidney Program, Associate Physician, Brigham and Women’s Hospital, and Associate Professor of Medicine, Harvard Medical School, Boston, Massachusetts, USA.

The researchers are currently in discussions with a pharmaceutical firm for the screening of drugs that could possibly target and shut-off the fibrosis-causing SCs in chronic organ disease incidence. “We wanted to know if eradication of this very small population of SCs would improve organ function, and both kidney and heart were completely protected from developing fibrosis-related complications (e.g. kidney and heart failure),” commented Dr Humphreys.

“This provides an important proof of principal that drugs that target the SCs could be therapeutic.”

(Image: freeimages.com)

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