Execution: the Critical “What’s Next?” in Strategic Human Resource Management

The Human Resource Planning Society’s 1999 State of the Art/Practice (SOTA/P) study was conducted by a virtual team of researchers who interviewed and surveyed 232 human resource and line executives, consultants, and academics worldwide. Looking three to five years ahead, the study probed four basic topics: (1) major emerging trends in external environments, (2) essential organizational capabilities, (3) critical people issues, and (4) the evolving role of the human resource function. This article briefly reports some of the study’s major findings, along with an implied action agenda – the “gotta do’s for the leading edge. Cutting through the complexity, the general tone is one of urgency emanating from the intersection of several underlying themes: the increasing fierceness of competition, the rapid and unrelenting pace of change, the imperatives of marketplace and thus organizational agility, and the corresponding need to buck prevailing trends by attracting and, especially, retaining and capturing the commitment of world-class talent. While it all adds up to a golden opportunity for human resource functions, there is a clear need to get to get on with it – to get better, faster, and smarter – or run the risk of being left in the proverbial dust. Execute or be executed

Itaconate Links Inhibition of Succinate Dehydrogenase with Macrophage Metabolic Remodeling and Regulation of Inflammation

Remodeling of the tricarboxylic acid (TCA) cycle is a metabolic adaptation accompanying inflammatory macrophage activation. During this process, endogenous metabolites can adopt regulatory roles that govern specific aspects of inflammatory response, as recently shown for succinate, which regulates the pro-inflammatory IL-1β-HIF-1α axis. Itaconate is one of the most highly induced metabolites in activated macrophages, yet its functional significance remains unknown. Here, we show that itaconate modulates macrophage metabolism and effector functions by inhibiting succinate dehydrogenase-mediated oxidation of succinate. Through this action, itaconate exerts anti-inflammatory effects when administered in vitro and in vivo during macrophage activation and ischemia-reperfusion injury. Using newly generated Irg1(−/−) mice, which lack the ability to produce itaconate, we show that endogenous itaconate regulates succinate levels and function, mitochondrial respiration, and inflammatory cytokine production during macrophage activation. These studies highlight itaconate as a major physiological regulator of the global metabolic rewiring and effector functions of inflammatory macrophages