Albeit in a state of cell cycle arrest, senescent cells can remain metabolically active and secrete cytokines, chemokines, growth factors and reactive oxygen species (ROS). This SASP is induced by myriad stressors, including cancer treatments, pro-inflammatory cytokines and ROS. Although the precise role of senescence in the intersection of CVD and cancer development is unclear, SASP is hypothesized to be involved. In a review study published in Frontiers in Cardiovascular Medicine in 2021, Le detailed how SASP instigates CVD and the molecular mechanisms by which SASP is implicated in tumorigenesis. The functional role of senescence in cancer is controversial. SASP can be induced in both normal and cancer cells by stress, oncogenes or therapy. Interestingly, chemotherapy-induced senescence can condition senescent cancer cells to acquire senescence-associated stemness, which causes them to escape cell cycle arrest, become proliferative and promote both CVD and cancer. On the other hand, several murine model and human specimen studies have demonstrated that senescent cardiovascular cells accumulate at the site of CVD and promote atherosclerosis, heart failure, arterial stiffness and hypertension. A key observation noted by Le is that SASP can lead to CVD as well as cancer. Conversely, both cancer and CVD provide feedback loops to activate SASP.

In a review study published in Frontiers in Cardiovascular Medicine in 2021, Le detailed how SASP instigates CVD and the molecular mechanisms by which SASP is implicated in tumorigenesis. The functional role of senescence in cancer is controversial. SASP can be induced in both normal and cancer cells by stress, oncogenes or therapy. Interestingly, chemotherapy-induced senescence can condition senescent cancer cells to acquire senescence-associated stemness, which causes them to escape cell cycle arrest, become proliferative and promote both CVD and cancer. On the other hand, several murine model and human specimen studies have demonstrated that senescent cardiovascular cells accumulate at the site of CVD and promote atherosclerosis, heart failure, arterial stiffness and hypertension. A key observation noted by Le is that SASP can lead to CVD as well as cancer. Conversely, both cancer and CVD provide feedback loops to activate SASP. “Understanding the regulation of SASP is the key to understand not only the interconnections between cancer and CVD but also age-related diseases such as diabetes mellitus, Alzheimer’s disease, cataract and chronic obstructive pulmonary disease,” said Le. Cancer treatments improve patient survival. However, the side effects can decrease patients’ quality of life. In many cases, the cancer cells become resistant to therapies and evolve to become even more aggressive, which defeats the purpose of the therapy. One interesting case in point is the strategy used in therapy-induced senescence whereby the therapy triggers cellular senescence to impede the growth of cancer cells. Surprisingly, therapy-induced senescence can induce SASP, which can lead to more potent cancer growth. Strategies focusing on modulating SASP appear to hold greater promise in the future for advances in the treatment of both CVD and cancer.