Telomeres at the ends of each chromosome shorten with every cell division, reaching their Hayflick limit after which time their length becomes insufficient and cells enter senescence.
Some cancer cells possess a mutation to their telomerase RNA template that allows them to bypass senescence checkpoint and continue dividing without becoming tumorous.
1. It Prevents Cancer
Like the plastic tips that keep shoelaces from unraveling, telomeres serve as protective structures at the ends of chromosomes in cells. Over time, however, their protective structures shorten over time until reaching a critical threshold, prompting cells to self-destruct. But stem cells contain an enzyme known as telomerase to counteract this shortening and restore their ability to divide. Scientists have discovered that increasing levels of this telomerase in stem cells may reverse cell senescence and restore their ability to divide.
Cancer cells lack this protection function and develop unlimited proliferative capability, leading to tumor development over time. They grow at an unchecked pace while normal cells succumb to genetic instability or senescence over time.
Researchers have discovered that patients suffering from autoimmune diseases such as rheumatoid arthritis, chronic fatigue syndrome and fibromyalgia often have shorter telomeres in their lymphocytes – this decrease can be tied to increased DNA damage and accelerated aging processes, poorer immune responses as well as less production of blood cells and natural killer (NK) cells.
An important cellular mechanism of aging is unrepaired DNA damage caused by cell division. Over time, this leads to the degradation of hTERT protein that signaled end of cycle for cell cycle; without its signalling function hTERT degrades and more damage occurs as more chromosomes become vulnerable; ultimately all DNA becomes too damaged for replication anymore and eventually cells no longer reproduce themselves.
Normal cells employ an alternative telomere maintenance system distinct from telomerase to counter this tendency. This mechanism involves the formation of heterodimers between hTERT and its catalytic subunit, hTR. When bound, this heterodimer adds an array of repetitive sequences of nucleotides at the ends of each chromosome – though this cannot prevent shortening entirely.
2. It Reverses Aging
Multicellular organisms undergo cell aging due to gradual loss of telomere length over time, caused by cell division. When this threshold is reached, end-to-end chromosome fusion occurs, leading to extensive cell death (apoptosis). Most cells use an enzyme known as telomerase to counter this process by adding short DNA repeats onto each chromosome’s ends – effectively prolonging lifespan by keeping its integrity.
However, over time telomerase becomes less effective; after several divisions most cells find that their telomeres become too short to allow further DNA replication and stop dividing or self-destruct.
Telomerase provides one means by which to combat this cellular aging process by adding short DNA repeats to each of our chromosomes with every cell division, but its effectiveness is restricted by an intrinsic brake encoded within the reverse transcriptase component hTERT’s RNA template RNA template; research led by Yinnan Chen, Joshua Podlevsky and Dhenugen Logeswaran has unlocked this mechanism and revealed how its activation and purpose-related limitations limit its functioning limiting its functionality; their discovery provides a roadmap for supercharging telomerase activity to better combat shortening and reverse aging effects in human adult stem cells.
3. It Reverses Diabetes
Scientists have developed an innovative technique for lengthening the ends of chromosomes containing our genetic information without having to replicate an entire chromosome each time a cell divides. They use modified messenger RNA (mRNA), which carries instructions for making proteins. They modified it so it contained instructions for producing an enzyme called telomerase which counteracts short chromosomal ends which cause cells to stop dividing and eventually die out.
Telomerase-mimetic drugs that activate mRNA could lengthen chromosome ends by adding small DNA repeats each time cells divide, giving cells more time for reproduction and potentially slowing or even reversing aging processes. A laboratory study published today in FASEB Journal has verified this new strategy as effective.
Researchers used an artificial chromosome to generate the mRNA for telomerase, and then introduced it into human cells for culture and testing, including DNA analysis and cell division. Researchers observed that those carrying this artificial chromosome had significantly longer chromosome ends compared to control cells without this gene.
Researchers also explored which factors might impede telomerase activity and discovered that TCAB1 interacts with both of telomerase’s main subunits hTERT and hTR to promote their assembly into an effective holoenzyme. It has been shown to bind directly to telomeric repeats through its WD-40 domain as well as an hTR-specific CAB-box sequence in its gene. Other binding partners for hTERT include chaperone HSP90/p23 as well as ATPases pontin/reptin/reptin/etc.
Studies have linked shorter leukocyte telomeres with type 1 and 2 diabetes. A recent research study of obese children revealed that their average white blood cell telomere lengths were significantly shorter at baseline compared with healthy children, yet increased over the six month weight management program and one year afterwards; suggesting reverse attrition associated with obesity.
4. It Prevents Heart Disease
Telomerase has already been proven effective at increasing mouse lifespan and may offer hope to those suffering from heart disease. Scientists at Spain’s National Cancer Research Centre (CNIO) have now made history by discovering that activating telomerase in specific organs, like the heart, increased survival rates after heart attacks.
Cardiovascular disease is one of the leading causes of death globally and one of its primary risk factors is aging. Over time, cells lose their ability to replicate, shortening telomeres until eventually prompting cell senescence and leading to cell loss which in turn triggers cardiovascular diseases. This results in decreased healthy and functioning cells and an increase in cardiovascular diseases as a direct result.
Researchers have linked telomere length with human cellular senescence and found that shorter telomeres are linked to an increase in chronic diseases like diabetes, obesity, cancer and non-vascular cardiovascular disease. Furthermore, some genetic mutations that reduce telomerase activity or accelerate shortening have been linked with dyskeratosis congenita, aplastic anemia or idiopathic pulmonary fibrosis – suggesting further links.
Prior studies with mice have demonstrated how complete removal of the telomerase gene results in atherosclerosis and reduced cardiac myocyte function, leading to cardiovascular complications. More recently, genome-wide association studies have confirmed that individuals with shorter leukocyte telomeres are at increased risk of ischemic heart disease.
5. It Prevents Alzheimer’s Disease
With every cell division, some genetic information is lost. To protect this vital data from being permanently erased, structures known as telomeres exist to add very short DNA repeats each time a cell divides – this eventually leads to their becoming short enough for the cell to stop dividing and enter senescence, contributing to inflammation that underlies many age-related illnesses like heart disease, diabetes, and Alzheimer’s.
Scientists have recently discovered that cells suffering from cellular senescence can be saved through an enzyme known as telomerase, which reverses it by replacing short DNA repeats that were lost every time cells split off from each other with new copies.
Scientists have recently made the discovery that telomerase activators extend cell lifespan and delay many diseases associated with aging such as cancer, cardiovascular disease, pulmonary fibrosis, autoimmune disorders and Alzheimer’s.
Blood cells from those living with Alzheimer’s disease exhibit shorter telomeres than healthy control subjects. This decrease is directly correlated to amyloid pathology within their brains as well as cognitive decline over two years in dementia patients, while treatment of AD patients using telomerase activators led to improved clinical symptoms.
Leukocyte telomere length correlates with severity of age-related macular degeneration (AMD), which affects an estimated 67 million people globally, according to a double-blind trial involving early AMD patients and telomerase activators significantly improving vision in them. Telomere dysfunction also correlates with oxidative stress – an indicator of heart disease risk; for instance in mouse models of cardiac ischaemia-reperfusion injury where length correlated with cellular senescence and decreased function – while activators improved cardiac function significantly while improving cardiac function significantly in human patients carrying mutations of an a-synuclein gene by significantly improving cardiac function overall.