The Journal Club returns live on our Facebook page on Wednesday 31st of March at 12:00 Eastern. This month we are taking a look at the new paper from Dr. Maria Blasco and team – Short and dysfunctional telomeres sensitize the kidneys to develop fibrosis .
For the Lifespan Heroes, you have the option to join us live on the call and join in directly with the discussion. The zoom details are below:
Time: Mar 31, 2021 12:00 PM Eastern Time
Meeting link is here
Meeting ID: 858 3373 6161
Accumulation of short telomeres is a hallmark of aging. Mutations in telomerase or telomere-binding proteins lead to telomere shortening or dysfunction and are at the origin of human pathologies known as ‘telomere syndromes’, which are characterized by loss of the regenerative capacity of tissues and fibrotic pathologies. Here, we generated two mouse models of kidney fibrosis, either by combining telomerase deficiency to induce telomere shortening and a low dose of folic acid, or by conditionally deleting Trf1, a component of the shelterin telomere protective complex, from the kidneys. We find that short telomeres sensitize the kidneys to develop fibrosis in response to folic acid and exacerbate the epithelial-to-mesenchymal transition (EMT) program. Trf1 deletion in kidneys led to fibrosis and EMT activation. Our findings suggest that telomere shortening or dysfunction may contribute to pathological, age-associated renal fibrosis by influencing the EMT program.