Heat shock protein responses after dermatologic laser and energy-based device treatments: A wavelength-oriented review of HSP70, HSP27, and HSP47 in skin remodeling

Dermatologic lasers and energy-based devices induce controlled tissue stress through photothermal, photomechanical, photochemical, or mixed mechanisms. The resulting response determines whether treatment produces adaptive repair, collagen remodeling, pigment modulation, vascular injury, or excessive damage. This review summarizes evidence for heat shock protein (HSP) responses after dermatologic laser and energy-based device exposure, with emphasis on HSP70, HSP27, and HSP47. A wavelength-oriented evidence map was developed from PubMed-oriented searches, manual source verification, and a targeted reference audit. Direct core evidence was defined as heat shock protein measurement after laser exposure in skin, skin explants, or skin-relevant cell systems. HSP70 or HSP72 is the best-supported marker after controlled thermal laser exposure, particularly after ablative fractional carbon dioxide laser treatment, 1550 nm nonablative fractional resurfacing, 1540 nm Er:glass treatment, 1064 nm neodymium-doped yttrium aluminum garnet (Nd:YAG) treatment, 815 nm diode laser treatment, and 1850 nm thermal preconditioning. HSP47 is best interpreted as a collagen-remodeling companion marker rather than a general acute heat shock marker. In contrast, HSP27 or HSPB1 is biologically relevant for cytoskeletal stabilization, oxidative stress control, autophagy, and inflammatory regulation, but remains insufficiently mapped after dermatologic laser exposure. A focused source audit of the public GSE168760 transcriptomic dataset after ablative fractional laser treatment found no meaningful HSPA1A/HSPA1B or HSPB1/HSP27 transcript induction, but showed an early HSPA6/HSPA7 response and persistent serpin family H member 1 (SERPINH1)/HSP47 upregulation. These findings support HSP70 as the most defensible current molecular marker of controlled laser-induced thermal stress and viable repair responses in skin, while identifying HSP27 as a priority marker for future laser studies.