MOTS-c · research summary

LAT1-mediated delivery of engineered R13A-MOTS-c attenuates radiation-induced lung injury via Nrf2 activation and mitochondrial protection.

Redox biology · 2026. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.

Study type

Preclinical study involving human serum samples, in vitro cell culture experiments, and in vivo mouse models.
“In vitro experiments revealed that R13A-MOTS-c suppressed inflammatory responses, oxidative damage, and mitochondrial impairment in MLE-12 cells. In vivo studies demonstrated that daily intraperitoneal administration of R13A-MOTS-c (5 mg/kg for 2 weeks) effectively mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in C57BL/6 mice exposed to 20 Gy thoracic irradiation.”

Subjects

Human thoracic cancer patients, MLE-12 mouse lung epithelial cells, and C57BL/6 mice.
“we collected serum samples from 10 thoracic cancer patients who developed RILI after radiotherapy (RILI) and 10 thoracic cancer patients who did not develop RILI after radiotherapy as controls.”

Sample size

10 patients per group for human serum analysis; n=5 mice per group for in vivo studies; n=3 for most in vitro experiments.
“Data are presented as mean ± SD (n = 10).”

Duration

Two weeks for the in vivo mouse treatment period.
“In vivo studies demonstrated that daily intraperitoneal administration of R13A-MOTS-c (5 mg/kg for 2 weeks) effectively mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in C57BL/6 mice exposed to 20 Gy thoracic irradiation.”

Reported findings

R13A-MOTS-c enters cells via LAT1-mediated transport, which is confirmed by competition assays and knockdown experiments.
“Functional uptake assays, including competition with canonical LAT1 substrates (leucine, BCH) and LAT1 knockdown experiments, further confirmed that R13A-MOTS-c enters cells via LAT1-mediated transport.”
R13A-MOTS-c mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in mice.
“In vivo studies demonstrated that daily intraperitoneal administration of R13A-MOTS-c (5 mg/kg for 2 weeks) effectively mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in C57BL/6 mice exposed to 20 Gy thoracic irradiation.”
The protective effects of R13A-MOTS-c are dependent on the activation of the Nrf2 signaling pathway.
“Mechanistically, R13A-MOTS-c activated the Nrf2 signaling pathway, as evidenced by increased nuclear translocation of Nrf2 and upregulation of its downstream targets gene.”

Source: PubMed 42142418 · DOI 10.1016/j.redox.2026.104204 · all study summaries

Study type

Preclinical study involving human serum samples, in vitro cell culture experiments, and in vivo mouse models.

“In vitro experiments revealed that R13A-MOTS-c suppressed inflammatory responses, oxidative damage, and mitochondrial impairment in MLE-12 cells. In vivo studies demonstrated that daily intraperitoneal administration of R13A-MOTS-c (5 mg/kg for 2 weeks) effectively mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in C57BL/6 mice exposed to 20 Gy thoracic irradiation.”

Duration

Two weeks for the in vivo mouse treatment period.

“In vivo studies demonstrated that daily intraperitoneal administration of R13A-MOTS-c (5 mg/kg for 2 weeks) effectively mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in C57BL/6 mice exposed to 20 Gy thoracic irradiation.”

Reported findings

R13A-MOTS-c enters cells via LAT1-mediated transport, which is confirmed by competition assays and knockdown experiments.

“Functional uptake assays, including competition with canonical LAT1 substrates (leucine, BCH) and LAT1 knockdown experiments, further confirmed that R13A-MOTS-c enters cells via LAT1-mediated transport.”

R13A-MOTS-c mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in mice.

“In vivo studies demonstrated that daily intraperitoneal administration of R13A-MOTS-c (5 mg/kg for 2 weeks) effectively mitigated radiation-induced pulmonary inflammation, oxidative stress, and mitochondrial dysfunction in C57BL/6 mice exposed to 20 Gy thoracic irradiation.”

The protective effects of R13A-MOTS-c are dependent on the activation of the Nrf2 signaling pathway.

“Mechanistically, R13A-MOTS-c activated the Nrf2 signaling pathway, as evidenced by increased nuclear translocation of Nrf2 and upregulation of its downstream targets gene.”