Accelerated telomere shortening in rheumatic diseases: cause or consequence?

Abstract

Accelerated aging of the immune system (immune aging), represented by telomere shortening, has been implicated in a variety of rheumatic diseases. Studies addressing telomere shortening in rheumatic diseases so far yielded controversial results. The current review aims to provide an overview on the role of immune aging in a plethora of immune-mediated conditions including systemic sclerosis, rheumatoid arthritis, systemic lupus erythematosus and osteoarthritis. The main question this review aims to answer is whether rheumatic diseases cause accelerated aging or that accelerated aging drives rheumatic diseases.

Keywords::

• osteoarthritis
• rheumatoid arthritis
• SLE
• systemic sclerosis
• T cells
• telomeres

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• • Accelerated biological aging of the immune system is thought to correlate with diseases.

• • Telomere length and telomerase activity can be used to measure biological aging, and be compared with chronological age to compare rate of biological aging between healthy controls and patients.

• • The main question of this review is whether accelerated telomere shortening is a cause or consequence of disease.

• • The rheumatic diseases rheumatoid arthritis, systemic lupus erythmatosus, osteoarthritis and systemic sclerosis are used to review whether accelerated aging drives their development or whether their mere existence causes accelerated aging. Literature indicates that telomere length often is shorter in patients, but does not correlate with disease duration.

• • Healthy relatives of patients have similarly short telomere length compared with patients.

• • There seems to be a prelude of accelerated telomere shortening, which poses some at a higher risk for disease development. Thus, accelerated telomere shortening is suggested to be a cause and not a consequence of disease development.