The growing incidence of obesity and related complications such as cardiomyopathy and nephropathy remains a global health
challenge. Many pathophysiological factors including inflammation, oxidative stress and endothelial dysfunction are implicated in obesity-
induced abnormalities in the heart and kidney. Moreover, obesity and nutrient-overload are associated with the activation of different
inflammatory/oxidative signaling pathways such as endoplasmic reticulum stress, nuclear factor-kappaB (NF-κB), toll-like-receptor-4
(TLR4) and the renin-angiotensin-aldosterone system (RAAS). The pathophysiological role of RAAS, TLR4 and NF-κB in perturbing
physiological milieu is well acknowledged. Several pharmacological agents have been formulated to target one or more of these pathways.
Although significant strides have been made in elucidating mechanisms implicated in obesity-related cardio-renal diseases, much
still has to be done. The pathophysiology of cardiomyopathy and nephropathy is complex and multifaceted. Besides NF-κ B, TLR4,
RAAS and inflammatory mediators such as cytokines and chemokines, a wide spectrum of different factors including, the environment,
diets, lifestyles, genetics and epigenetics are also involved. With such multifactorial etiology, it remains a daunting challenge to identify
the factor(s) that initiate the activation and propagation of adverse stimuli that eventually lead to cardiomyopathy and/or nephropathy in
obese individuals. Similarly, the mechanisms of such activation and propagation should be clearly elucidated. Should these hurdles be
overcome, there would be a greater likelihood for the development of more-effective therapeutic strategies for the prevention, treatment
and management of obesity-induced cardiomyopathy and nephropathy. The present review examines the role of inflammation, oxidative
stress and endothelial dysfunction in obesity-induced abnormalities in heart and kidney.