Scientific Profile – Judith Campisi

//Scientific Profile – Judith Campisi

Scientific Profile – Judith Campisi

Judith Campisi

 

For all that we at NEM talk about aging and healthcare, people rarely can put a face to the researchers that make these scientific breakthroughs possible. Through our scientific profiles, we will introduce you to some of the most famous and interesting scientists working today, and the incredible research that they do. 

Judith Campisi is one of the world’s foremost aging scientists. Her work into cellular senescence has helped us understand how aging can be the root cause of so many diseases, including cancer and Alzheimer’s. After a career spent at the New York University of Stony Brook and Harvard Medical School, she is now the head of the Campisi Lab at the Buck Institute, which is known for its research into longevity. 

Her research focuses on the topic of cellular senescence, which is when cells stop dividing after having reached the end of their lifespan (1). This happens for lots of reasons, such as the loss of their telomeres (which was discussed in the article Hallmarks of aging, part two), or by being put under stress from the external environment (such as an increase in stress-related hormones, or cells being subjected to the toxins in cigarette smoke) (2). At the start of your life, senescence is a good thing. Although they are no longer able to renew, the cells have become senescent because they were damaged- to continue to allow them to keep dividing would mean to introduced potentially mutated cells into the body.  The act of making cells senescent is a major way that our body prevents tumours from growing (3)

In addition, senescent cells themselves aren’t useless- Campisi’s research found that the “zombie” cells could promote wound healing (4). However, as time goes on and senescent cells build up, they can start to contribute to some pretty nasty things, from tissue degradation, inflammation and age-related diseases like cancer (2). In this way, what starts as an anti-cancer mechanism can actually end up causing it (3).

Two of her most cited and important pieces of research are summarised below, covering the story from how senescence is linked to cancer, chronic inflammation and other age-related diseases.

The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression (5)

Cells change as they become senescent, getting larger and altering how it looks and the chemicals that it puts out into its environment. This is called a change in its phenotype, or its physical characteristics. It was originally believed that these cells were benign, not really doing anything to affect the cells they were neighbouring. However, this research reveals that this is not the case. Whilst cellular senescence is initially something that stops tumours being produced, some senescent cells can produce secretions that cause the cells around them to become more cancerous. They do this by releasing chemicals that make the other cells grow and divide more quickly, increasing the size and speed of the tumour, or with chemicals that make the other cells more aggressive and likely to invade other tissues. Senescent cells accumulate with age, and thus cancer becomes more likely with age too as more and more senescent cells contribute to a pro-cancer environment. 

Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases (6)

Inflammation is a normal process in our bodies, often occurring in response to a wound and lessening after a couple of days when the wound is healed. However, chronic inflammation doesn’t diminish over time. It stays as low, constant background inflammation in the body, and can be caused by various things including cellular senescence. It is linked to age related changes in the body, such as our metabolism becoming less efficient, and our immune system becoming less effective. It’s also linked to age-related diseases, like type 2 diabetes and cardiovascular disease. However, the paper also states that there is a light at the end of the tunnel- some anti-inflammatory medications are already in use for chronic diseases, like statins for blocking the inflammatory action of bad cholesterol, and drugs that specifically act against the senescence-associated secretory phenotype are also in the pipeline. 

These incredible pieces of research from the Campisi lab helped to change scientific understanding of senescence and give us another piece of the puzzle in what contributes to aging and the things that can be done to stop it. 

References

  1. Hayflick L. THE LIMITED IN VITRO LIFETIME OF HUMAN DIPLOID CELL STRAINS. Exp Cell Res. 1965 Mar;37:614–36.
  2. Campisi J, d’Adda di Fagagna F. Cellular senescence: when bad things happen to good cells. Nat Rev Mol Cell Biol. 2007 Sep;8(9):729–40.
  3. Schosserer M, Grillari J, Breitenbach M. The Dual Role of Cellular Senescence in Developing Tumors and Their Response to Cancer Therapy. Front Oncol. 2017 Nov 23;7:278.
  4. Demaria M, Ohtani N, Youssef SA, Rodier F, Toussaint W, Mitchell JR, et al. An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA. Dev Cell. 2014 Dec 22;31(6):722–33.
  5. Coppé J-P, Desprez P-Y, Krtolica A, Campisi J. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annu Rev Pathol. 2010;5:99–118.
  6. Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci. 2014 Jun;69 Suppl 1:S4–9.

 

2021-07-23T12:28:16+01:00