Stress repair mechanism activity explains inflammation and apoptosis


A review of modern evidence using Internet resources has identified the Stress Repair Mechanism (SRM) postulated by Hans Selye in 1951. SRM activity regulates thrombin generation to govern tissue maintenance, tissue repair, hemodynamic physiology, inflammation, and apoptosis. Thrombin utilizes ATP to energize coagulation, capillary hemostasis, chemotaxis, immune activity, mitosis, metabolism, angiogenesis, and the release of chemokines, cytokines, bradykinins, and prostaglandins that enable cell-to-cell communications, promote perfusion, loosen cell connections, and sensitize nociceptors during tissue repair. The orchestration of these diverse activities by the SRM explains the disparate elements of the inflammation syndrome, including dolor (pain), rubor (redness), calor (heat), tumor (swelling), and Functio laesa (loss of function). Inflammation resolves as tissue repair nears completion and declining SRM activity restores thrombin to maintenance levels. As thrombin levels decline below a critical threshold, repair cells undergo apoptosis and clots disintegrate. Apoptosis shrinks granulation tissues to enable wound closure. Apoptosis also facilitates embryological development. Occult systemic SRM hyperactivity due to sepsis, surgery, trauma, chemicals, pain, fear, and emotional memories causes inflammatory effects that manifest as the fever, edema, malignancy, organ disruption, eclampsia, Multi-System Organ Failure (MS-OF), Systemic Inflammatory Response Syndrome (SI-RS), Adult Respiratory Distress Syndrome (ARDS), Disseminated Intravascular Coagulation (DIC) and other pathologies.

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Coleman, L. (2012) Stress repair mechanism activity explains inflammation and apoptosis. Advances in Bioscience and Biotechnology, 3, 459-503. doi: 10.4236/abb.2012.324065.

Conflicts of Interest

The authors declare no conflicts of interest.


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