Pulmonary fibrosis

Pulmonary fibrosis (literally “scarring of the lungs”) is a respiratory disease in which scars are formed in the lung tissues, leading to serious breathing problems. Scar formation, the accumulation of excess fibrous connective tissue (the process called fibrosis), leads to thickening of the walls, and causes reduced oxygen supply in the blood. As a consequence patients suffer from perpetual shortness of breath.

Reversal by Providing the Missing microRNAs.

Recent observations indicate that fibrosis, aging and abnormal wound healing are linked to the down expression of specific genes.
More specifically, researchers have shown that the expression of MicroRNAs of the miR-29 family are significantly reduced in fibrotic lungs. They show that miR-29 levels are inversely correlated with the severity of the fibrosis.
(http://www.ncbi.nlm.nih.gov/pubmed/20971881, Am. J. Respir. Cell. Mol. Biol. 2011 Aug)

Embryonic Stem Cells express miR29 as can be seen in this extensive publication of the microRNAs released by them: http://www.genesil.com/docs/Embryonic%20stem%20cell-specific%20MicroRNAs.pdf

For this reason we first observed reversal of keloids on wounds as a positive side-effect of our anti-aging Stem Cells treatment. Then we observed that fibrotic livers and lungs have improved function following our Stem Cells therapy.

Patient Data

Our most recent pulmonary fibrosis patient had been diagnosed with a progressive form of the disease over one year ago.

Here is his progress report after having received 10 Embryonic Stem Cell injections:

• Feeling fantastic.

• Arthritic pain in my neck and back has cleared up completely.

• I am looking younger.

• One lady thought my younger brother was my father LOL.

• The scar tissue (Dupuytren’s contracture) on my hand is clearing up, so … I know the scar tissue in my lungs is       being repaired in the same way.

• Cough is gone.

• Atrial premature beats are gone.

His oxygenation capacity started to improve following his third injection.
The Dupuytren’s contracture is linked to the same fibrosis condition and can also be reversed with embryonic stem cell therapy.


Our fibrosis reversal protocol includes a recommended minimum dose of 6 Stem Cells injections to initiate the reversal process, following by regular “maintenance” injections.

If you want to experience the Embryonic Stem Cells Pulmonary fibrosis program we have developed, please fill out the ‘contact us form’

Then we will contact you shortly with all the information.


Age of Donor Affects Stem Cell Effectiveness in Repairing Lung Damage from Pulmonary Fibrosis

Miller School of Medicine researchers have found that the age of a donor mouse affects the ability of its mesenchymal stem cells (MSCs) to repair damage to the lungs caused by pulmonary fibrosis.

Their laboratory study, published recently in Translational Research, has important implications for clinical stem cell treatments in older patients with damaged and scarred lung tissue caused by smoking or other conditions.

“Donor Stem Cells from younger mice were effective in preventing damage when infused into older mice at the same time as a disease-causing agent,” said Marilyn K. Glassberg, M.D., professor of medicine, surgery and pediatrics, Director of the Interstitial Lung Disease Program, Director of Pulmonary Diseases at the Interdisciplinary Stem Cell Institute, and Vice-Chair of Medicine for Diversity and Innovation. “However, donor MSCs from older mice had virtually no effect.”

Because there are no drugs to reverse the damage from pulmonary fibrosis, researchers have studied the potential for autologous MSCs from a patient’s own body as a possible strategy for repairing lung tissue, said Glassberg, who was a senior author of the study, “Therapeutic benefits of young, but not old, adipose-derived mesenchymal stem cells in a chronic mouse model of bleomycin-induced pulmonary fibrosis.”

Jun Tashiro, M.D., M.P.H., surgical resident, and Sharon J. Elliot, Ph.D., research associate professor of medicine, were lead authors of the Miller School study, and other co-authors were David J. Gerth, M.D., assistant professor of surgery; Xiaomei Xia, research associate in medicine; Simone Pereira-Simon, research associate in surgery; Rhea Choi, M.D./Ph.D. student; Paola Catanuto, Ph.D., senior research associate of surgery; Shahriar Shahzeidi, M.D., clinical assistant professor of pediatrics; and Rahil H. Shah, student assistant. Also contributing to the study were Rebecca L. Toonkel, M.D., of Florida International University; and Fadi El Salem, M.D., of the Icahn School of Medicine at Mount Sinai.

“Our study found that the age of the donor animal is important,” said Glassberg. “This would indicate that it’s unlikely that infusions of autologous stem cells from the body of an older patient would be effective in treating pulmonary disease.”

A series of laboratory studies in the late 1990s and early 2000s indicated that stem cells could repair lung damage in mice given bleomycin (BLM)-induced pulmonary fibrosis. “These studies used young mice as the model,” said Glassberg. “But data showed that these mice would be able to repair the damage without being given stem cells.”

To develop a better representative model for pulmonary fibrosis, Elliot was able to obtain old mice – equivalent to 70 human years – through a grant from the National Institutes of Aging (NIH). When these mice received stem cell infusions from old donor mice, there was no reduction in fibrosis or other signs of improvement. However, when old mice received MSCs from young donor mice, their lung damage did improve. Importantly, when young mice received old donor MSCs their lung repair was altered. Studies are ongoing to determine what old donor cells have or lack compared to young donor cells that render them ineffective.

“We plan to continue to develop more representative models of human pulmonary fibrosis,” said Glassberg. “Our goal is not only to develop a preventive model of disease but also to search for a way to offer safe and effective clinical treatments for patients with this deadly disease.”

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