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Pharmaceuticals (Basel). 2017 Dec 23;11(1). doi: 10.3390/ph11010002.

Roles of Heat Shock Proteins in Apoptosis, Oxidative Stress, Human Inflammatory Diseases, and Cancer.

Pharmaceuticals (Basel, Switzerland)

Paul Chukwudi Ikwegbue, Priscilla Masamba, Babatunji Emmanuel Oyinloye, Abidemi Paul Kappo

Affiliations

  1. Biotechnology and Structural Biochemistry (BSB) Group, Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3886, South Africa. [email protected].
  2. Biotechnology and Structural Biochemistry (BSB) Group, Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3886, South Africa. [email protected].
  3. Biotechnology and Structural Biochemistry (BSB) Group, Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3886, South Africa. [email protected].
  4. Department of Biochemistry, Afe Babalola University, PMB 5454, Ado-Ekiti 360001, Nigeria. [email protected].
  5. Biotechnology and Structural Biochemistry (BSB) Group, Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3886, South Africa. [email protected].

PMID: 29295496 PMCID: PMC5874698 DOI: 10.3390/ph11010002

Abstract

Heat shock proteins (HSPs) play cytoprotective activities under pathological conditions through the initiation of protein folding, repair, refolding of misfolded peptides, and possible degradation of irreparable proteins. Excessive apoptosis, resulting from increased reactive oxygen species (ROS) cellular levels and subsequent amplified inflammatory reactions, is well known in the pathogenesis and progression of several human inflammatory diseases (HIDs) and cancer. Under normal physiological conditions, ROS levels and inflammatory reactions are kept in check for the cellular benefits of fighting off infectious agents through antioxidant mechanisms; however, this balance can be disrupted under pathological conditions, thus leading to oxidative stress and massive cellular destruction. Therefore, it becomes apparent that the interplay between oxidant-apoptosis-inflammation is critical in the dysfunction of the antioxidant system and, most importantly, in the progression of HIDs. Hence, there is a need to maintain careful balance between the oxidant-antioxidant inflammatory status in the human body. HSPs are known to modulate the effects of inflammation cascades leading to the endogenous generation of ROS and intrinsic apoptosis through inhibition of pro-inflammatory factors, thereby playing crucial roles in the pathogenesis of HIDs and cancer. We propose that careful induction of HSPs in HIDs and cancer, especially prior to inflammation, will provide good therapeutics in the management and treatment of HIDs and cancer.

Keywords: apoptosis; cancer; heat shock proteins; inflammation; reactive oxygen species; tumour necrosis factor-α

Conflict of interest statement

The authors declare no conflict of interest.

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