Limits...
ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury.

Minutoli L, Puzzolo D, Rinaldi M, Irrera N, Marini H, Arcoraci V, Bitto A, Crea G, Pisani A, Squadrito F, Trichilo V, Bruschetta D, Micali A, Altavilla D - Oxid Med Cell Longev (2016)

Bottom Line: In normal conditions, ROS mediate important beneficial responses.Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation.Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy.

ABSTRACT
Ischemia and reperfusion (I/R) causes a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to the ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, and inflammatory responses to cell death. In normal conditions, ROS mediate important beneficial responses. When their production is prolonged or elevated, harmful events are observed with peculiar cellular changes. In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation. The mechanisms underlying the activation of NLRP3 are several and not completely elucidated. It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation. Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated.

No MeSH data available.


Related in: MedlinePlus

Schematic representation of ischemia/reperfusion injury and of potential therapeutic strategies to modulate oxidative stress and/or related NLRP3 activation.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4835650&req=5

fig1: Schematic representation of ischemia/reperfusion injury and of potential therapeutic strategies to modulate oxidative stress and/or related NLRP3 activation.

Mentions: The imbalance between ROS formation and the detoxifying action of these oxidizing radicals induces a cellular condition, called oxidative stress [11]. In particular, ROS, during I/R, promote tissue inflammation and activate immune response through NLRP3 inflammasome [11] (Figure 1).


ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury.

Minutoli L, Puzzolo D, Rinaldi M, Irrera N, Marini H, Arcoraci V, Bitto A, Crea G, Pisani A, Squadrito F, Trichilo V, Bruschetta D, Micali A, Altavilla D - Oxid Med Cell Longev (2016)

Schematic representation of ischemia/reperfusion injury and of potential therapeutic strategies to modulate oxidative stress and/or related NLRP3 activation.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4835650&req=5

fig1: Schematic representation of ischemia/reperfusion injury and of potential therapeutic strategies to modulate oxidative stress and/or related NLRP3 activation.
Mentions: The imbalance between ROS formation and the detoxifying action of these oxidizing radicals induces a cellular condition, called oxidative stress [11]. In particular, ROS, during I/R, promote tissue inflammation and activate immune response through NLRP3 inflammasome [11] (Figure 1).

Bottom Line: In normal conditions, ROS mediate important beneficial responses.Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation.Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy.

ABSTRACT
Ischemia and reperfusion (I/R) causes a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to the ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, and inflammatory responses to cell death. In normal conditions, ROS mediate important beneficial responses. When their production is prolonged or elevated, harmful events are observed with peculiar cellular changes. In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation. The mechanisms underlying the activation of NLRP3 are several and not completely elucidated. It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation. Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated.

No MeSH data available.


Related in: MedlinePlus