Background While photochemical damage mechanisms have been extensively characterized, thermal damage from infrared (IR) radiation and environmental heat persists as an underappreciated pathophysiological entity. Current photoprotection standards focus exclusively on ultraviolet (UV) blocking, leaving skin vulnerable to thermally-induced aging and systemic deterioration. Objective To systematically delineate skin thermal damage as distinct from photoaging through comparative molecular energetics analysis, propose an operational scientific definition, and elucidate the paradigm shift from "photon blocking" to "systemic conditioning" for effective thermal protection. Methods Comprehensive literature synthesis (2022-2025) focusing on epigenetic aging studies, TRPV1 thermosensory mechanisms, heat shock protein dynamics, and multi-targeted pharmacological interventions. Results Thermal damage operates through physical energy accumulation (molecular vibrational excitation) rather than photochemical bond cleavage, with TRPV1/Ca 2+ /HSF1 signaling constituting a pathway independent of UV-induced DNA damage. Recent evidence demonstrates that chronic heat exposure accelerates epigenetic aging by 14 months—equivalent to smoking effects (Choi 2025)—through DNAmAge acceleration. Notably, IR effects exhibit dose-dependent biphasicity: low-dose photobiomodulation (<10 J/cm 2 ) confers beneficial preconditioning via mild HSP induction, whereas high-dose thermal accumulation (>42°C tissue temperature) triggers destructive protein denaturation and MMP-1 upregulation. Conclusions Skin thermal damage represents a "physical dissolution" process characterized by cumulative internal structural disruption, necessitating protection strategies fundamentally different from UV blocking. Traditional Chinese Medicine offers unique advantages through multi-targeted "conditioning" of cellular resilience mechanisms, aligning with the holistic requirements of thermal protection.
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Yang et al. (2026) studied this question.
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