In short
Telomerase is an enzyme that adds telomere repeat sequences back onto the ends of chromosomes, counteracting the shortening that normally occurs with cell division.
Telomerase is a ribonucleoprotein — it carries its own RNA template (TERC) that it uses, together with its catalytic protein subunit (TERT), to synthesize new telomeric DNA. This lets a cell replenish telomere length that would otherwise erode with each division.
Most human somatic cells silence TERT expression after early development, so telomerase activity is low in adult tissue outside of stem cells, immune cells during activation, and the germline. This silencing is thought to be a tumor-suppressive trade-off: unlimited replicative capacity is exactly what a cancer cell needs, and roughly 85–90% of human cancers reactivate telomerase (most of the remainder use an alternative telomere-lengthening mechanism).
This trade-off is why telomerase activation is not a straightforward longevity strategy. A rare inherited disease, dyskeratosis congenita, is caused by telomerase mutations and causes premature aging-like symptoms, showing that too little telomerase is harmful — but reactivating telomerase broadly in adult tissue raises cancer-risk concerns that have kept it out of mainstream human longevity therapeutics. Some gene-therapy telomerase-activation experiments have extended lifespan in mice without increased cancer, but this remains preclinical work, not a human intervention.