In order to investigate the effects of lipopolysaccharide (LPS) on the mitochondrial signaling pathway in muscle cells of Tan sheep, M longissimus dorsi muscles from six-month-old Tan sheep were aged at 4 ℃ for 0, 6, 12, 24 and 72 h postmortem and evaluated for pH, ATP content, cell apoptosis rate, cell apoptosis-related enzyme activity, succinatedehydrogenase (SDH) activity, citrate synthase (CS) activity, B-cell lymphoma 2 (Bcl-2) family protein contents, and cytochrome c (Cyt-c) and cysteinyl aspartate specific proteinase 3 (Caspase-3) expression levels. The results showed that the apoptosis rate and Bcl-2-associated X protein (Bax)/Bcl-2 ratio in the control and LPS-induced groups were significantly increased during postmortem aging (P < 0.05). The activities of Caspase-3 and Caspase-9 increased first and then decreased. After LPS treatment, the activities of Caspase-3 and Caspase-9 were higher than those in the control group at all time points. The pH, Cyt-c reduction level and mitochondrial ATP content were significantly decreased overall (P < 0.05). The relative expression level of Cyt-c was significantly increased in both groups at 12 h postmortem, and decreased during 24–72 h in the LPS group. The content of Caspase-3 activated fragment protein in the LPS treatment group was higher than that in control group at the same time points. In conclusion, LPS could activate Caspase-3 and Caspase-9, and reduce the mitochondrial content of ATP and consequently energy metabolism level, thus affecting the activities of SDH and CS, promoting the release of Cyt-C, and increasing Bax/Bcl-2 ratio, and finally inducing cell apoptosis through the mitochondrial signaling pathway.

This research investigated the relationship between mitochondrial damage and meat tenderness of Tan sheep during postmortem aging. The M. Longissimus dorsi muscles from six-month-old Tan sheep were divided into lipopolysaccharide (LPS) treatment and blank control groups. Mitochondrial reactive oxygen species (ROS) content, membrane potential, mitochondrial permeability transition pore (MPTP) openness, mitochondrial swelling, pH, cooking loss, texture, moisture distribution, shear force and myofibril fragmentation index (MFI) in each group were measured at 0, 6, 12, 24, and 72 hours postmortem. The results showed that during postmortem aging, MPTP openness gradually increased in both groups. ROS content, cooking loss rate and MFI value showed an increasing trend as well. Mitochondrial membrane potential, pH, elasticity, T₂₂ peak area and shear force showed a decreasing trend. Hardness, chewability and cohesiveness increased at first and then decreased. Therefore, disruption of oxidative homeostasis in muscle cells of Tan sheep resulted in an increase of ROS content, which caused mitochondrial damage by inducing the opening of MPTP and decreasing mitochondrial membrane potential. Moreover, the structural changes of myofibrils shortened the gap between muscle protein molecules, resulting in increased water loss rate and poorer water retention in muscles, promoting the process of myofibril fragmentation and improving the tenderness of Tan sheep meat. Correlation analysis showed that mitochondrial damage and tenderization occurred simultaneously during the postmortem aging of Tan sheep meat, and the more serious the mitochondrial damage was, the better the tenderness was.

Signal transducer and activator of transcription 3 (STAT3) exists in the cytoplasm, nucleus, mitochondria, and mitochondria associated endoplasmic reticulum membranes, which is a signal transduction protein involved in various physiological processes such as cell proliferation, differentiation, migration, and immune regulation. This article provides an overview of the structures and types of STAT3 and the pathways through which STAT3 enters mitochondria, and elaborates on the regulatory effect of STAT3 on cellular homeostasis including the anti-apoptotic effect mediated by endoplasmic reticulum Ca²⁺ transport, the mechanism of action in maintaining mitochondrial function, and the regulatory mechanism on lipid synthesis and catabolism. Furthermore, this paper explores the regulatory mechanism of STAT3 on meat color from the perspective of regulating hematopoietic stem cells, skeletal muscle, mitochondrial homeostasis, and lipid synthesis and metabolism in order to provide a theoretical reference for improving meat color.

Tenderness is one of the most important indicators to judge meat quality, and it is also the most important sensory index for consumers to choose meat. Postmortem muscle undergoes complex biochemical processes, and apoptosis is considered to be a key biochemical pathway to regulate postmortem muscle tenderization. Lysosomes are rich in cathepsins, and a large amount of cathepsins are released after lysosomal membrane permeabilization, which activates the caspase cascade through the intrinsic lysosomal-mitochondrial pathway, triggering apoptosis and consequently accelerating postmortem muscle tenderization. This article introduces the action mechanism and metabolic processes of lysosomes and elaborates the activation pathways of lysosomal membrane permeabilization through reactive oxygen species (ROS), sphingosine, B-cell lymphoma-2 (Bcl-2) and p53 proteins. Furthermore, it explores the pathway for the involvement of lysosomes in apoptosis, and summarizes the regulatory mechanism of lysosomes on muscle tenderization from the perspectives of the release of cathepsins and Ca²⁺, caspase activation and iron-induced oxidative stress. We hope that this review can provide a theoretical reference for improving meat tenderness.

The endoplasmic reticulum is a key site for calcium storage, lipid synthesis, protein synthesis, transport and folding, and it performs several critical biological functions. Ca²⁺ imbalance, protein overload, and hypoxic conditions can disrupt cellular homeostasis, leading to an increase in unfolded and misfolded proteins and triggering endoplasmic reticulum stress. Prolonged endoplasmic reticulum stress not only activates the signaling pathways of protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6) within the endoplasmic reticulum, but also mediates apoptosis by participating in the activation of B cell lymphoma 2 interacting mediator of cell death (Bim) in the cytoplasm. This review covers the mechanism underlying endoplasmic reticulum overload response and describes the pathways by which the endoplasmic reticulum mediates apoptosis including the signaling sensors (PERK, IRE1, and ATF6) within the endoplasmic reticulum, the Bim pathway in the cytoplasm, and the interplay between endoplasmic reticulum stress and oxidative stress. Furthermore, this review summarizes the mechanism by which endoplasmic reticulum stress regulates muscle tenderization from four perspectives: modification of myofibrillar proteins by reactive oxygen species, Ca²⁺ release, apoptosis, and the anti-apoptotic effects of heat shock proteins. It is our hope that this review will provide a more comprehensive scientific basis for improving muscle tenderness.

Postmortem muscle is highly susceptible to oxidative conditions, thus leading to deterioration of meat quality in terms of tenderness, color, and water-holding capacity (WHC). Therefore, the regulation of the oxidation mechanism is a major concern in research on postmortem meat quality. Reactive nitrogen species (RNS) are free radicals and nitro compounds with high oxidation activity derived from the interaction between nitric oxide (NO) and compounds including reactive oxygen species (ROS). RNS not only regulates mitochondria to promote cellular metabolic function, but also mediates mitochondrial damage to induce cell apoptosis, thereby regulating the quality of postmortem meat. Relevant research results need to be summarized urgently. Therefore, this paper provides an overview of the production and metabolism of RNS in cells, elaborates on the mechanism by which RNS regulates normal physiological functions of cells through mitochondria, induces cell apoptosis through causing mitochondrial damage and mediates oxidation mechanism including lipid peroxidation and protein oxidation, and discusses the mechanism by which RNS affect the tenderness, color, and WHC of postmortem muscle. We anticipate that this review will provide a theoretical reference for improving postmortem ageing.