Apoptosis and its role in postmortem meat tenderness: A comprehensive review

Area of Science:

• Muscle biology
• Meat science
• Biochemistry

Background:

• Meat tenderness is vital for consumer acceptance and economic value.
• Postmortem muscle undergoes significant biochemical changes, including cell death, influencing meat quality.
• Endogenous enzymatic degradation of myofibrillar proteins is the primary mechanism for meat tenderization.

Purpose of the Study:

• To systematically review cell death types (apoptosis, autophagy, necrosis) in postmortem muscle.
• To elucidate the molecular mechanisms of apoptosis and its pathways affecting meat tenderness.
• To discuss factors influencing apoptosis in postmortem muscle.

Main Methods:

• Literature review of existing research on postmortem muscle cell death and meat tenderization.
• Systematic summary of apoptosis pathways: mitochondrial, death receptors, and endoplasmic reticulum stress.
• Discussion of factors impacting apoptosis: reactive oxygen species (ROS), heat shock proteins, calcium/calpains, and Bcl-2 family proteins.

Main Results:

• Apoptosis is a major contributor to postmortem meat tenderization.
• The mitochondrial pathway is the predominant apoptotic mechanism.
• Caspase activation, triggered by apoptosis, leads to myofibrillar protein degradation.

Conclusions:

• Apoptosis significantly improves meat tenderness through caspase-mediated protein hydrolysis.
• Understanding postmortem apoptosis provides a foundation for developing novel meat tenderization strategies.
• Further research into apoptosis mechanisms can optimize meat quality and processing techniques.