Blood-borne Aging Process Linked to This Protein
Study Identifies Key Molecule in Systemic Aging Process
A groundbreaking study conducted by a team of researchers at Korea University's College of Medicine has shed light on the mechanisms behind the systemic spread of aging and senescence. The study, led by senior author Ok Hee Jeon, reveals that a specific chemical form of the HMGB1 protein, known as ReHMGB1, acts as a molecular messenger, transmitting "senescence signals" from cell to cell through the bloodstream.
Senescent cells, which are cells that have stopped dividing due to stress or damage but are not dead, release a cocktail of substances called the senescence-associated secretory phenotype (SASP). These substances can damage nearby healthy cells and cause premature aging. However, ReHMGB1, unlike other forms of HMGB1, can travel through the bloodstream and induce senescence in distant cells.
ReHMGB1 binds to a receptor called RAGE, which triggers inflammatory signaling pathways such as JAK/STAT and NF-κB. These pathways reinforce cellular senescence and inflammation, effectively promoting aging processes in distant tissues. If scientists can interrupt these signals, they might be able to slow the aging process systemically, not just in one organ.
The study supports the emerging view that aging is not just wear and tear, but a coordinated process driven by signals that travel through the body. In older mice, ReHMGB1 levels in the blood are naturally higher compared to younger ones. Blocking ReHMGB1 through antibodies in middle-aged mice with muscle injuries resulted in fewer senescent cells, stronger muscle regeneration, and improved grip strength and endurance.
On the other hand, injecting ReHMGB1 into young mice led to increased senescence markers in various tissues and reduced muscle performance. The oxidized form of HMGB1, OxHMGB1, has no effect on triggering senescence in cells.
The findings were reported in the journal Metabolism. However, ReHMGB1 is unstable in the bloodstream and difficult to target precisely, requiring a treatment that is safe enough to block harmful forms without interfering with the protein's normal roles.
In conclusion, ReHMGB1 is a critical systemic pro-aging molecule that spreads senescence and inflammation across multiple tissues by activating key inflammatory pathways downstream of RAGE, thereby reinforcing and propagating cellular aging beyond local tissue environments. This provides a mechanistic basis for the systemic nature of aging and may offer targets for interventions to slow or mitigate age-related tissue decline.
The study reveals that aging signals are not confined to individual cells but can be systemically transmitted via the blood, with ReHMGB1 acting as a key driver. This discovery offers promising avenues for future research into therapies that could potentially slow the aging process and improve overall health in later life.
- The study identifies a key molecule, ReHMGB1, involved in the systemic spread of aging, which is a significant discovery in the field of medicine and health-and-wellness.
- The research sheds light on the mechanisms behind the aging process, highlighting the role of ReHMGB1 in transmitting "senescence signals" from cell to cell through the bloodstream.
- By understanding the role of ReHMGB1 in aging, science might be able to develop treatments that could potentially slow the aging process systemically, improving health and wellness in later life.
- The study indicates that aging is driven by signals that travel through the body, not just wear and tear, and opens up new avenues for research in health and science, particularly concerning aging and the future of health-and-wellness.
