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Facial aging is characterized by progressive macroscopic, histological, and molecular changes. Due to its regenerative and rejuvenating properties, the use of platelet-rich plasma (PRP) as a facial antiaging agent has gained popularity over the last decade. In order to gather and evaluate the latest evidence focusing on the effect of PRP on facial skin rejuvenating, a search through MEDLINE (PubMed) using relevant keywords, inclusion, and exclusion criteria was performed. A total of 539 articles were initially retrieved, and from those, 16 were included in the review. Treatment protocols comprised the use of PRP both in monotherapy and in combination with other substances and by means of direct injection or topical application following skin permeation. The selected studies presented high variability regarding PRP preparation methods, administration protocols, and results assessment. In most studies, PRP seemed to improve to some degree the signs of facial aging, such has wrinkles, skin quality, and pigmentation, accompanied by significant histological and molecular responses. Optimizing treatment protocols should be the next step in assessing the full potential of PRP.

The myocardial response to acute stretch consists of a two-phase increase in contractility: an acute increase by the Frank-Starling mechanism and a gradual and time-dependent increase in force generated known as the slow force response (SFR). The SFR is actively modulated by different signaling pathways, but the role of protein kinase G (PKG) signaling is unknown. In this study we aim to characterize the role of the PKG signaling pathway in the SFR under normal and ischemic conditions. Rabbit papillary muscles were stretched from 92 to 100% of maximum length (Lmax) under basal conditions, in the absence (1) or presence of: a PKG agonist (2) and a PKG inhibitor (3); under ischemic conditions in the absence (4) or presence of: a PKG agonist (5); a nitric oxide (NO) donor (6) and a phosphodiesterase 5 (PDE5) inhibitor (7). Under normoxia, the SFR was significantly attenuated by inhibition of PKG and remained unaltered with PKG activation. Ischemia induced a progressive decrease in myocardial contractility after stretch. Neither the PKG agonist nor the NO donor altered the myocardial response to stretch under ischemic conditions. However, the use of a PDE5 inhibitor in ischemia partially reversed the progressive deterioration in contractility. PKG activity is essential for the SFR. During ischemia, a progressive decline in the force is observed in response to acute myocardial stretch. This dysfunctional response can be partially reversed by the use of PDE5 inhibitors.