2026-10-10T06:00:51Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33810595 2026-09-15T17:32:40Z category_4 category_7 category_12 category_13 category_14 category_16 category_502 category_46 category_734 portal_5 item_type_3 month_year_09_2026

<p>Muscle contractile force raw data.</p> Jingwang Liu (24948190) Jiaxin Liu (833821) Tianyi He (1415218) Penghui Zhang (661086) Nan Zhao (351674) Maozheng Wei (15216974) Yuxin Guan (17021502) Peng Liu (120506) Shuang Zhao (484057) Xiuli Wang (151314) Biochemistry Medicine Cell Biology Genetics Molecular Biology Physiology Astronomical and Space Sciences not elsewhere classified Immunology Biological Sciences not elsewhere classified xlink "> tourniquet total mechanistic target sarcolemmal integrity disruption phosphorylated mechanistic target mechanical pain threshold improved motor performance lower limb ischemia induced muscle contraction early functional impairment abnormally elevated perfusion 3 hours followed protective actions may left hindlimb ischemia esk mitigates acute autophagy dysregulation may hindlimb ischemia hindlimb perfusion gastrocnemius muscle functional outcomes 24 hours protective effect tissue injury results showed related markers related genes present study partially abrogated nerve stimulation mouse model inflammatory response findings indicate esk increased esk attenuated esk alone chloroquine phosphate 6 levels <div><p>Tourniquet-associated lower limb ischemia-reperfusion can induce skeletal muscle inflammation, edema, and early functional impairment, in which autophagy dysregulation may be involved. The present study was designed to investigate the effects of esketamine (ESK) on skeletal muscle injury following lower limb ischemia-reperfusion in mice and its relationship with autophagy regulation. A mouse model of left hindlimb ischemia for 3 hours followed by 24 hours of reperfusion was established, and changes in hindlimb perfusion, functional outcomes, tissue injury, inflammatory response, and autophagy-related markers were examined after intervention with ESK alone or in combination with chloroquine phosphate (CQ). The results showed that ESK attenuated the abnormally elevated perfusion after reperfusion, improved motor performance and partial muscle contractile function, yet exerted limited effects on mechanical pain threshold and nerve stimulation-induced muscle contraction. Concurrently, ESK alleviated histological damage, edema, and sarcolemmal integrity disruption in the gastrocnemius muscle, reduced serum Tumor Necrosis Factor-alpha and Interleukin-6 levels, and downregulated the expression of several inflammation-related genes. With respect to autophagy, ESK increased the microtubule-associated protein 1 light chain 3 II/I ratio while decreasing sequestosome 1 levels and the phosphorylated mechanistic target of rapamycin/total mechanistic target of rapamycin ratio; these protective effects were partially abrogated by CQ. Collectively, these findings indicate that ESK mitigates acute-phase skeletal muscle injury and improves selected early functional outcomes after lower limb ischemia-reperfusion in mice, and that its protective actions may be associated with suppression of inflammation and modulation of autophagy.</p></div> 2026-09-15T17:32:34Z Dataset Dataset 10.1371/journal.pone.0358125.s004 https://figshare.com/articles/dataset/_p_Muscle_contractile_force_raw_data_p_/33810595 CC BY 4.0