Anti-Aging Potential of Platelet Rich Plasma (PRP): Evidence from Osteoarthritis (OA) and Applications in Senescence and Inflammaging

Abstract

Aging and age-related changes impact the quality of life (QOL) in elderly with a decline in movement, cognitive abilities and increased vulnerability towards age-related diseases (ARDs). One of the key contributing factors is cellular senescence, which is triggered majorly by DNA damage response (DDR). Accumulated senescent cells (SCs) release senescence-associated secretory phenotype (SASP), which includes pro-inflammatory cytokines, matrix metalloproteinases (MMPs), lipids and chemokines that are detrimental to the surrounding tissues. Chronic low-grade inflammation in the elderly or inflammaging is also associated with cellular senescence and contributes to ARDs. The literature from the last decade has recorded the use of platelet rich plasma (PRP) to combat senescence and inflammation, alleviate pain as an analgesic, promote tissue regeneration and repair via angiogenesis—all of which are essential in anti-aging and tissue regeneration strategies. In the last few decades, platelet-rich plasma (PRP) has been used as an anti-aging treatment option for dermatological applications and with great interest in tissue regeneration for orthopaedic applications, especially in osteoarthritis (OA). In this exploration, we connect the intricate relationship between aging, ARDs, senescence and inflammation and delve into PRP’s properties and potential benefits. We conduct a comparative review of the current literature on PRP treatment strategies, paying particular attention to the instances strongly linked to ARDs. Finally, upon careful consideration of this interconnected information in the context of aging, we suggest a prospective role for PRP in developing anti-aging therapeutic strategies.

The implications of Brain-derived neurotrophic factor in the biological activities of platelet-rich plasma.

“…This receptor is expressed in synoviocytes, chondrocytes, osteoclasts, and osteoblasts [22,[77][78][79][80]. In addition, although not directly linked with OA pathogenesis, BDNF might have potential therapeutic activities through the antiinflammatory, anti-apoptotic, and antioxidant actions and modulation of autophagy in the affected OA tissue damage, that leads to the joint healing process [73,81].…”

“…interaction between BDNF and Trk-B receptor in neurons led to the activation of signaling cascades mainly ruled by PI3K, MAPK, PLCγ, and GTPases enzymes that ultimately lead to cell growth & dendrite branching, cell survival and synaptic plasticity[72,73]. Of interest, BDNF signaling through PI3K leads to further phosphorylation of AKT kinase inhibiting the intrinsic and extrinsic pathways and further neuronal apoptosis.…”

Translating Senotherapeutic Interventions into the Clinic with Emerging Proteomic Technologies

“…Pharmacological compounds [20] and biologics, such as platelet-rich plasma [21], have been identified as candidate senotherapeutics for the treatment of aging and the pathologies of aging. Within this context, we highlight small-molecule senotherapeutic compounds that have demonstrated notable efficacy in preclinical studies, positioning them as promising candidates for future clinical investigation.…”