Abstract
Patients with diabetes are over-represented among the total cases reported with “idiopathic” pulmonary fibrosis (IPF). This raises the question, whether this is an association only or whether diabetes itself can cause pulmonary fibrosis. Recent studies in mouse models of type 1 and type 2 diabetes demonstrated that diabetes causes pulmonary fibrosis. Both types of diabetes trigger a cascade, starting with increased DNA damage, an impaired DNA repair, and leading to persistent DNA damage signaling. This response, in turn, induces senescence, a senescence-associated-secretory phenotype (SASP), marked by the release of pro-inflammatory cytokines and growth factors, finally resulting in fibrosis. Restoring DNA repair drives fibrosis into remission, thus proving causality. These data can be translated clinically to patients with type 2 diabetes, characterized by long-term diabetes and albuminuria. Hence there are several arguments, to substitute the term “idiopathic” pulmonary fibrosis (IPF) in patients with diabetes (and exclusion of other causes of lung diseases) by the term “diabetes-induced pulmonary fibrosis” (DiPF). However, future studies are required to establish this term and to study whether patients with diabetes respond to the established therapies similar to non-diabetic patients.
| Original language | English |
|---|---|
| Article number | 765201 |
| Journal | Frontiers in Endocrinology |
| Volume | 12 |
| DOIs | |
| State | Published - 25 Nov 2021 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- diabetes
- hyperglycemia
- persistent DNA damage signaling
- pulmonary fibrosis
- senescence
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