Unveiling the interactions among BMPR-2, ALK-1 and 5-HTT genes in the pathophysiology of HAPE

Ali, Zahara; Waseem, Mohammad; Kumar, Rahul; Pandey, Priyanka; Mohammad, Ghulam; Pasha, M. A. Qadar

doi:10.1016/j.gene.2016.05.016

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…Recently, much attention has been given to acquire knowledge on the genetic basis of HAPE [10]. When an individual has previous experience of HAPE, the prevalence of having such episodes in the future is highly increased (>60%) in high-altitudes indicating individual susceptibility and genetic basis of HAPE [6].…”

Section: Geneticsmentioning

confidence: 99%

“…HAPE is precipitated by a severe and abrupt change in barometric pressure [9]. Subsequently, decreased partial pressure of oxygen causes uneven vasoconstriction resulting in exaggerated capillary pressure, increased capillary permeability, and fluid collection in the lungs [9,10]. Exposure to hypoxia increases pulmonary arterial systolic pressure (PASP) that is directly proportional to the degree of hypoxia [11] and altitude [12].…”

Section: Introductionmentioning

confidence: 99%

“…They also described an association between viral upper airway infection with HAPE susceptibility [15,20,21]. Recently much attention has been given to acquiring knowledge on the genetic basis of HAPE, where genome-wide association and candidate gene molecular approaches are commonly used [10]. When an individual has previous experience of HAPE, the prevalence of having such episodes in the future is highly increased (>60%) in high-altitudes indicating individual susceptibility and genetic basis of HAPE [6].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Patchy Vasoconstriction Versus Inflammation: A Debate in the Pathogenesis of High Altitude Pulmonary Edema

Kandel

Mishra

Gautam

et al. 2020

Cureus

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High altitude pulmonary edema (HAPE) occurs in individuals rapidly ascending at altitudes greater than 2,500 m within one week of arrival. HAPE is characterized by orthopnea, breathlessness at rest, cough, and pink frothy sputum. Several mechanisms to describe the pathophysiology of HAPE have been proposed in different kinds of literature where most of the mechanisms are reported to be activated before a drop in oxygen saturation levels. The majority of the current studies favor diffuse hypoxic pulmonary vasoconstriction (HPV) as a pathophysiological basis for HAPE. However, some of the studies described inflammation in the lungs and genetic basis as the pathophysiology of HAPE. So, there is a major disagreement regarding the exact pathophysiology of HAPE in the current literature, which raises a question as to what is the exact pathophysiology of HAPE. So, we reviewed 23 different articles which include clinical trials, review articles, randomized controlled trials (RCTs), and original research published from 2010 to 2020 to find out widely accepted pathophysiology of HAPE. In our study, we found out sympathetic stimulation, reduced nitric oxide (NO) bioavailability, increased endothelin, increased pulmonary artery systolic pressure (PASP) resulting in diffuse HPV, and reduced reabsorption of interstitial fluid to be the most important determinants for the development of HAPE. Similarly, with the evaluation of the role of inflammatory mediators like C-reactive protein (CRP) and interleukin (IL-6), we found out that inflammation in the lungs seems to modulate but not cause the process of development of HAPE. Genetic basis as evidenced by increased transcription of certain gene products seems to be another promising hypoxic change leading to HAPE. However, comprehensive studies are still needed to decipher the pathophysiology of HAPE in greater detail.

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Section: Geneticsmentioning

confidence: 99%